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HORMONES OF THE ENDOCRINE SYSTEM. HORMONES OF THE PITUITARY. NEUROHYPOPHYSIS--POSTERIOR PITUITARY ADENOHYPOPHYSIS--ANTERIOR PITUITARY. HORMONES OF THE NEUROHYPOPHYSIS. STORES AND SECRETES NEUROHORMONES PRODUCED BY HYPOTHALAMUS ANTIDIURETIC HORMONE OXYTOCIN. ANTIDIURETIC HORMONE. ADH

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hormones of the pituitary
HORMONES OF THE PITUITARY
  • NEUROHYPOPHYSIS--POSTERIOR PITUITARY
  • ADENOHYPOPHYSIS--ANTERIOR PITUITARY
hormones of the neurohypophysis
HORMONES OF THE NEUROHYPOPHYSIS
  • STORES AND SECRETES NEUROHORMONES PRODUCED BY HYPOTHALAMUS
  • ANTIDIURETIC HORMONE
  • OXYTOCIN
antidiuretic hormone
ANTIDIURETIC HORMONE
  • ADH
  • VASOPRESSIN
  • PREVENTS DIURESIS (LOSS OF URINE)
  • CONSTRICTS ARTERIOLES AND RAISES BLOOD PRESSURE
  • SYNTHESIZED IN SUPRAOPTIC NUCLEI OF HYPOTHALAMUS
  • CARRIED IN HYPOTHALAMOHYPOPYSEAL TRACT
  • STORED IN AXON TERMINALS IN PITUITARY
antidiuretic effect
ANTIDIURETIC EFFECT
  • AFFERENT VAGAL NERVES
  • DROP IN PRESSURE STIMULATES ADH SECRETION
  • INCREASE IN PRESSURE INHIBITS SECRETION
factors that increase adh secretion
FACTORS THAT INCREASE ADH SECRETION
  • EMOTIONAL STRESS
  • PHYSICAL STRESS
  • BLOOD VOLUME
  • INCREASED PLASMA OSMOTIC PRESSURE
  • DECREASED EXTRACELLULAR FLUID VOLUME
  • STRENUOUS EXERCISE
  • NICOTINE AND BARBITUATES
factors that decrease adh secretion
FACTORS THAT DECREASE ADH SECRETION
  • DROP IN PLASMA OSMOTIC PRESSURE
  • INCREASED EXTRACELLULAR FLUID VOLUME
  • ALCOHOL
diabetes insipidus
DIABETES INSIPIDUS
  • POLYURIA
  • POLYDYPSIA
  • LOSS OF ADH RELEASE
  • IMPAIRED WATER CONSERVATION
  • EXCESSIVE WATER LOSS IN URINE
oxytocin
OXYTOCIN
  • WOMEN
  • MEN
oxytocin in women
OXYTOCIN IN WOMEN
  • STIMULATES SMOOTH MUSCLE IN UTERUS
  • PROMOTES LABOR AND DELIVER
  • STIMULATES MYOEPITHELIAL CELLS OF MAMMARY GLANDS
oxytocin in males
OXYTOCIN IN MALES
  • UNCERTAIN
  • STIMULATES SMOOTH MUSCLE CONTRACTIONS IN DUCTUS DEFERENS AND PROSTATE
oxytocin and sex
OXYTOCIN AND SEX
  • AROUSAL AND ORGASM
  • EMISSION
  • CONTRACTIONS THAT PROMOTE SPERM TRANSPORT
hormones of the hypothalamus adenohypophysis
ADENOHYPOPHYSEAL HORMONES

TSH

ACTH

FSH

LH

PRL

GH

MSH

LIPOTROPIN

RELEASING AND INHIBITING

HORMONES FROM THE

HYPOTHALAMUS

TRH

CRH

GnRH

GnIH

PRH/PIH

GH-RH/SOMATOSTATIN

HORMONES OF THE HYPOTHALAMUS & ADENOHYPOPHYSIS
thyroid stimulating hormone
THYROID STIMULATING HORMONE
  • THYROTROPIN
  • RELEASE REGULATED BY THYROTROPIN RELEASING HORMONE (TRH)
  • TARGET CELLS IN THYROID
  • TRIGGERS RELEASE OF THYROID HORMONE
adrenocorticotropic hormone
ADRENOCORTICOTROPIC HORMONE
  • DERIVED FROM PROOPIMELANOCORTIN
  • INCREASES SECRETION OF ADRENAL HORMONES
  • BINDS TO MELANOCYTES AND INCREASE PIGMENTATION OF SKIN
other substances derived from proopimelanocortin
OTHER SUBSTANCES DERIVED FROM PROOPIMELANOCORTIN
  • LIPOTROPINS
  • BETA ENDORPHINS
  • MELANOCYTE STIMULATING HORMONE
lipotropins
LIPOTROPINS
  • SECRETED FROM SAME CELLS AS ACTH
  • BIND TO MEMBRANE RECEPTORS OF ADIPOSE CELLS
  • CAUSE FAT BREAKDOWN & RELEASE OF FATTY ACIDS INTO CIRCULATION
beta endorphins
BETA ENDORPHINS
  • SAME EFFECT AS OPIATES
  • IMPORTANT FOR ANALGESIA IN RESPONSE TO STRESS AND EXERCISE
  • MAY BE INVOLVED IN BODY TEMPERATURE FOOD INTAKE WATER BALANCE
  • STRESS INCREASES SECRETION ALONG WITH ACTH
melanocyte stimulating hormone
MELANOCYTE STIMULATING HORMONE
  • BINDS TO MELANOCYTES
  • STIMULATES DEPOSITION OF MELANIN
  • NOT WELL UNDERSTOOD IN HUMANS
  • IMPORTANT REGULATOR IN OTHER VERTEBRATES
  • PRODUCED IN PARS INTERMEDIA IN HUMANS PARS INTERMEDIA MERGES WITH PARS DISTALIS
relationship between melanocyte stimulating hormone and acth
RELATIONSHIP BETWEEN MELANOCYTE STIMULATING HORMONE AND ACTH
  • MSH IS SECRETED ALONG WITH ACTH
  • USUALLY NOT IN QUANTITIES LARGE ENOUGH TO HAVE A SIGNIFICANT EFFECT
  • MAY BE SIGNIFICANT IN ADDISON’S DISEASE
gonadotropins1
HORMONES PROMOTE GROWTH AND FUNCTION OF GONADS

LUTEINIZING HORMONE

FOLLICLE STIMULATING HORMONE

GONADOTROPINS
prolactin in females
PROLACTIN IN FEMALES
  • STIMULATES THE DEVELOPMENT OF DUCT SYSTEM IN MAMMARY GLANDS WITH OTHER HORMONES
  • STIMULATES MILK PRODUCTION
  • USUALLY INHIBITED BY PROLACTIN INHIBITING HORMONE
  • STIMULATED BY PROLACTIN RELEASING HORMONE
prolactin in males
PROLACTIN IN MALES
  • MAKES INTERSTITIAL CELLS MORE RESPONSIVE TO LUTEINIZING HORMONE
growth hormone
GROWTH HORMONE
  • SECRETION STIMULATED BY GROWTH HORMONE RELEASING HORMONE
  • SECRETION INHIBITED BY GROWTH HORMONE INHIBITING HORMONE/SOMATOSTATIN
growth hormone1
GROWTH HORMONE
  • STIMULATES GROWTH OF CARTILAGE AND BONE
  • INDIRECT EFFECTS
  • DIRECT EFFECTS
indirect effects
INDIRECT EFFECTS
  • SOMATOMEDINS /INSULIN-LIKE GROWTH FACTORS
  • PEPTIDE HORMONES
  • BIND TO MEMBRANE RECEPTORS
  • SKELETAL MUSCLE, CARTILAGE AND OTHER TARGET CELLS
direct effects
DIRECT EFFECTS
  • STIMULATES STEM CELL DIVISION AND GROWTH OF DAUGHTER CELLS
effects of growth hormone on metabolism
EFFECTS OF GROWTH HORMONE ON METABOLISM
  • INCREASED PROTEIN SYTHESIS
  • INCREASED MOBILIZATION OF FATTY ACIDS FROM ADIPOSE TISSUE
  • INCREASED USE OF FATTY ACIDS FOR ENERGY
  • DECREASED USE OF GLUCOSE THROUGHOUT BODY
  • SPARING GLUCOSE FOR THE BRAIN
effects of growth hormone on protein synthesis
EFFECTS OF GROWTH HORMONE ON PROTEIN SYNTHESIS
  • AMINO ACID TRANSPORT AT THE CELL
  • PROTEIN SYNTHESIS BY RIBOSOMES
  • INCREASED LEVELS OF RNA
  • DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS
amino acid transport at the cell
AMINO ACID TRANSPORT AT THE CELL
  • ENHANCES TRANPORT OF AMINO ACIDS
  • WORKS WITH INSULIN
  • INCREASED AMINO ACID LEVELS LEAD TO INCREASED PROTEIN SYNTHESIS
protein synthesis by ribosomes
PROTEIN SYNTHESIS BY RIBOSOMES
  • DIRECT EFFECT ON RIBOSOMES
increased levels of rna
INCREASED LEVELS OF RNA
  • INCREASES TRANSCRIPTION RATE
  • OVER TIME INCREASES LEVELS OF RNA
  • INCREASED RNA MEANS INCREASED PROTEIN SYNTHESIS
decreased catabolism of proteins and amino acids
DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS
  • DECREASE IN BREAKDOWN OF PROTEINS TO AMINO ACIDS
  • DECREASE OF USE OF AMINO ACIDS FOR ENERGY SOURCE
  • MAY BE DUE TO MOBILIZATION OF FATTY ACIDS SPARING PROTEIN
effects of growth hormone on fat metabolism
EFFECTS OF GROWTH HORMONE ON FAT METABOLISM
  • CAUSE LIPOLYSIS AND THE RELEASE OF FATTY ACIDS INTO BODY FLUIDS AND CIRUCLATION
  • ENHANCES CONVERSION OF FATTY ACIDS TO ACETYL CO A
  • INCREASES USE OF ACETYL CO A FOR ENERGY
  • FAT METABOLISM FAVORED OVER CARBOHYDRATE AND PROTEIN METABOLISM
effects of growth hormone on carbohydrate metabolism
EFFECTS OF GROWTH HORMONE ON CARBOHYDRATE METABOLISM
  • DECREASES USE OF GLUCOSE FOR ENERGY
  • ENHANCES GLYGOGENESIS
  • DIMINISHES GLUCOSE UPTAKE BY CELLS
decreased use of glucose for energy
DECREASED USE OF GLUCOSE FOR ENERGY
  • PERHAPS DUE TO INCREASED MOBILIZATION AND UTILIZATION OF FATS
enhances glycogenogenesis
ENHANCES GLYCOGENOGENESIS
  • GLUCOSE WILL BE STORED AS GLYCOGEN
  • RESERVES RAPIDLY FILL UP
diminished glucose uptake by cells
DIMINISHED GLUCOSE UPTAKE BY CELLS
  • INITIAL INCREASED GLUCOSE UPTAKE
  • UNTIL GLYCOGEN RESERVE IS FILLED
  • THEN UPTAKE DIMINISHES
  • GREATLY INCREASED BLOOD GLUCOSE LEVELS
secretion of growth hormone
SECRETION OF GROWTH HORMONE
  • 3 NANOGRAMS IN ADULT
  • 5 NANOGRAMS IN CHILD
  • REGULATED BY GH-RH AND SOMATOSTATIN
hormones of the thyroid gland

HORMONES OF THE THYROID GLAND

THYROID HORMONE AND CALCITONIN

thyroid hormone
THYROID HORMONE
  • THYROXINE (T4 )
  • TRIIODOTHRYONINE (T3 )
importance of thyroglobulin
IMPORTANCE OF THYROGLOBULIN
  • GLYCOPROTEIN
  • CONTAINS 140 TYROSINE AMINO ACIDS
  • SUBSTRATE IODINE BINDS WITH
  • HORMONES FORM WITHIN THYROGLOBULIN MOLECULE
importance of iodine
IMPORTANCE OF IODINE
  • USED ONLY TO MAKE THYROID HORMONES
  • STORED IN THYROID
  • IDODIDE PUMP TRAPS IODIDE
the wedding of thyroglobulin and iodide ions
THE WEDDING OF THYROGLOBULIN AND IODIDE IONS
  • OCCURS AT THE COLLOID-CELL INTERFACE AS THYROGLOBULIN IS SECRETED
mit and dit
MIT AND DIT
  • MONOIODTYROSINE
  • DIIODOTYROSINE
  • THYROXINE
  • TRIIODOTHRYRONINE
thyroglobulin storage
THYROGLOBULIN STORAGE
  • IN COLLOID OF FOLLICLE
  • ONLY HORMONE STORED EXTRACELLULARLY
  • 1-3 MONTH SUPPLY IN COLLOID
release of thyroid hormone into the blood
RELEASE OF THYROID HORMONE INTO THE BLOOD
  • THYROGLOBULIN IS PICKED UP BY FOLLICULAR CELLS
  • LYSOSOMES FUSE WITH PINOCYTIC VESICLES
  • THYROXINE AND TRIIODOTHYRONINE ARE CLEAVED FROM THRYOGLOBULIN AND RELEASED
transport in the blood
TRANSPORT IN THE BLOOD
  • THRYOXINE BINDING GLOBULIN
  • ALBUMINS
thyroid hormones at the cells
THYROID HORMONES AT THE CELLS
  • ENTERS CELLS
  • BINDS WITH INTRACELLULAR PROTEIN RECEPTOR
  • THYROXINE HAS GREATER AFFINITY
importance of latency and duration of action
IMPORTANCE OF LATENCY AND DURATION OF ACTION
  • T4 -- TWO OR THREE DAY LATENT PERIOD
  • MAXIMUM ACTIVITY IN 10-12 DAYS
  • T3 --- 6 TO 12 HOURS
  • MAXIMUM ACTIVITY IN 2-3 DAYS
major effects of thyroid horomone
MAJOR EFFECTS OF THYROID HOROMONE
  • GROWTH IN CHILDREN
  • INCREASE IN METABOLIC RATE
effects on growth
EFFECTS ON GROWTH
  • LACK OF THRYOID HORMONE RETARDS GROWTH
  • EXCESS OF THYROID HORMONE ENHANCES GROWTH IN CHILD
  • CAUSES EPIPHYSEAL PLATES TO CLOSE PREMATURELY SO FINAL HEIGHT MAY BE SHORTENNED
generalized effects on metabolism
GENERALIZED EFFECTS ON METABOLISM
  • AFFECT METABOLISM OF ALMOST ALL CELLS OF BODY
  • CALORIGENIC EFFECT
effect of thyroid hormone on protein synthesis
EFFECT OF THYROID HORMONE ON PROTEIN SYNTHESIS
  • PHASE ONE--INCREASED TRANSLATION
  • PHASE TWO--INCREASED TRANSCRIPTION
effect of thyroid hormone on cellular enzyme systems
EFFECT OF THYROID HORMONE ON CELLULAR ENZYME SYSTEMS
  • INCREASED PROTEIN SYNTHEIS RESULTS IN INCREASED CELLULAR ENZYMES
  • AS MUCH AS 6 TIMES NORMAL
effects on cellular organelles
EFFECTS ON CELLULAR ORGANELLES
  • INCREASED ACTIVITY OF MITOCHONDRIA
  • INCREASED NUMBER OF MITOCHONDRIA
effects on active transport
EFFECTS ON ACTIVE TRANSPORT
  • Na-K ATPase PUMPS INCREASE
  • INCREAED TRANSPORT OF SODIUM AND POTASSIUM
effects on carbohydrate metabolism
EFFECTS ON CARBOHYDRATE METABOLISM
  • RAPID UPTAKE OF GLUCOSE
  • INCREASED GLYCOLYSIS
  • INCREASED GLUCONEOGENESIS
  • INCREASED GI ABSORPTION
  • INCREASED INSULIN SECRETION
effect on fat metabolism
EFFECT ON FAT METABOLISM
  • LIPOGENESIS
  • LIPOLYSIS
  • MOBILIZATION OF LIPIDS
effects on body mass
EFFECTS ON BODY MASS
  • INCREASED THYROID HORMONE DECREASES
  • DECREASED THYROID HORMONE INCREASES
effects on cardiovascular system
EFFECTS ON CARDIOVASCULAR SYSTEM
  • INCREASED OXYGEN DEMAND
  • INCREASED METABOLIC WASTE PRODUCTS
  • CAUSE VASODILATION
  • NEED FOR HEAT ELIMINATION ALSO CAUSES VASODILATION
  • CARDIAC OUTPUT CAN INCREASE BY 50%
effects on respiration
EFFECTS ON RESPIRATION
  • INCREASED OXYGEN DEMAND
  • INCREASED CARBON DIOXIDE LEVELS
  • ACTIVATE MECHANISMS THAT INCREASE THE RATE AND DEPTH OF RESPIRATION
effect on gastrointestinal tract
EFFECT ON GASTROINTESTINAL TRACT
  • INCREASE ABSORPTION RATE
  • INCREASES SECRETION OF DIGESTION JUICES
  • INCREASES MOTILITY OF GASTROINTESTINAL TRACT
  • TO MUCH MAY LEAD TO DIARRHEA
  • TO LITTLE CONSTIPATION
effect on the central nervous system
EFFECT ON THE CENTRAL NERVOUS SYSTEM
  • NORMAL AMOUNTS INCREASE CEREBRATION
  • TO LITTLE DECREASES CEREBRATION
  • TO MUCH -- EXTREME NERVOUSNESS, PSYCHONEUROTIC TENDENCIES, MUSLE TREMOR, TIREDNESS BUT INABILITY TO SLEEP
  • TO LITTLE -- MENTAL SLUGGISHNESS EXTREME SOMNOLENCE
secretion of thyroid hormone
SECRETION OF THYROID HORMONE
  • TSH FROM ADENOHYPOPHYSIS STIMULATES ITS SECRTION TRH STIMULATES TSH SECRETION
negative feedback controls of thyroid hormone release
NEGATIVE FEEDBACK CONTROLS OF THYROID HORMONE RELEASE
  • LONG FEED BACK LOOPS
  • SHORT FEEDBACK LOOPS
long feedback loop
LONG FEEDBACK LOOP
  • INHIBITORY EFFECTS OF TARGET ORGANS ON ADENOHYPOPHYSIS
  • THYROID HORMONES COULD ACT ON HYPOTHALAMUS AND INHIBIT SECRETION OF TRH
  • THYROID HORMONE COULD ACT ON ADENOHYPOPHYSIS AND INHIBIT ITS RESPONSE TO RELEASING HORMONES
thyroid stimulating hormone1
THYROID STIMULATING HORMONE
  • HIGH SECRETION OF TSH MAY INHIBIT SECRETION OF TRH
specific effects of tsh
SPECIFIC EFFECTS OF TSH
  • INCREASED PROTEOLYTIC ACTIVITY IN FOLLICLES
  • INCREASED RELEASE OF THYROID HORMONE INTO BLOOD STREAM
  • INCREASED TRAPPING OF IODIDE IONS
  • INCREASED IODINATION OF TYROSINE
  • INCREAS`E IN SIZE AND ACTIVITY OF FOLLICULAR CELLS
  • INCREASED NUMBER OF FOLLICULAR CELLS
regulation of thryoid hormone secretion
REGULATION OF THRYOID HORMONE SECRETION
  • TSH FROM PITUITARY STIMULATES SYNTHESIS AND RELEASE
  • TRH PROMOTES TSH RELEASE
  • NEGATIVE FEED BACK
calcitonin
CALCITONIN
  • POLYPEPTIDE
  • PRODUCED BY PARAFOLLICULAR CELLS
  • LOWERS BLOOD CALCIUM AND PHOSPHATE LEVELS
  • SUPRESSES BONE RESORPTION
  • INCREASES BONE FORMATION
  • IMPORTANT IN BONE REMODELING
how calcitonin reduces blood calcium levels
HOW CALCITONIN REDUCES BLOOD CALCIUM LEVELS
  • DECREASES OSTEOLYTIC EFFECT FAVORS DEPOSITION RATHER THAN RESORPTION
  • INCREASES ACTIVITY OF OSTEOBLASTS
  • PREVENTS FORMATION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS
children vs adults
CHILDREN VS ADULTS
  • MAJOR ROLE IN CHILD
  • MINOR ROLE IN ADULTS
regulation of calcitonin secretion
REGULATION OF CALCITONIN SECRETION
  • 10% RISE IN PLASMA CALCIUM LEVELS LEADS TO 3-6 TIMES MORE CALCITONIN
other important effects of calcitonin
OTHER IMPORTANT EFFECTS OF CALCITONIN
  • REDUCES LOSS OF BONE MASS DURING PROLONGED STARVATION LATE STAGES OF PREGNANCY
differences between calcitonin and parathyroid hormone
DIFFERENCES BETWEEN CALCITONIN AND PARATHYROID HORMONE
  • CALCITONIN MORE RAPID
  • SHORT TERM REGULATOR
regulation of secretion
REGULATION OF SECRETION
  • PLASMA LEVELS OF CALCIUM
  • HIGH CONCENTRATION -- INCREASED SECRETION
  • LOW CONCENTRATION -- DECREASED SECRETION
  • GASTRIN AND OTHER INTESTINAL HORMONES EFFECT SECRETION
parathyroid gland
PARATHYROID GLAND
  • SMALL FLATTENED GLANDS
  • POSTERIOR SURFACE OF THYROID GLAND
cells of parathyroid
CELLS OF PARATHYROID
  • CHIEF CELLS
  • OXYPHIL CELLS
parathyroid hormone
PARATHYROID HORMONE
  • PTH
  • POLYPEPTIDE
  • TWO OR THREE FORMS
  • PRINCIPAL CONTOLLER OF CALCIUM AND PHOSPHATE IN BLOOD
  • INCREASES PLASMA CONCENTRATION OF CALCIUM
  • DECREASES PLASMA CONCENTRATION OF PHOSPHORUS
pth effects on bone
PTH EFFECTS ON BONE
  • OSTEOLYTIC EFFECT (BONE RESORPTION)
  • PROLIFERATION OF OSTEOCLASTS
pth effect on osteoclasts
PTH EFFECT ON OSTEOCLASTS
  • IMMEDIATE ACTIVATION OF OSTEOCLASTS
  • PRODUCTION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS
effect of pth on the kidneys
EFFECT OF PTH ON THE KIDNEYS
  • EXCRETION AND REABSORPTION
  • ACTIVATION OF VITAMIN D
exretion and reabsorption
EXRETION AND REABSORPTION
  • IMMEDIATE AND RAPID LOSS OF PHOSPHATE IN KIDNEYS DUE TO DECREASED REABSORPTION OF PHOSPHATES
  • INCREASED REABSORPTION OF CALCIUM IN KIDNEYS
activation of vitamin d
ACTIVATION OF VITAMIN D
  • CALCITRIOL
  • IMPORTANT FOR DEPOSITION IN BONES PROMOTES CALCIFICATION
  • IMPORTANT FOR ABSORPTION OF CALCIUM IN GI TRACT
thymus
THYMUS
  • LOCATED UNDER MEDIASTINUM
  • RELATIVELY LARGE IN CHILDREN
  • REACHES GREATEST SIZE IN PUBERTY -- 40 g
  • BEGINS TO INVOLUTE ON ITSELF AFTER PUBERTY TO 12 g AT 50
  • ACCELERATED BY GLUCOCORTICOIDS AND SEX HORMONES
thymic hormones
THYMIC HORMONES
  • THYMOSIN ALPHA
  • THYMOSIN BETA
  • THYMOSIN V
  • THYMOPOIETIN
  • THYMULIN
  • AND SOME OTHERS
effects of thymosin
EFFECTS OF THYMOSIN
  • DEVELOPMENT OF B AND T LYMPHOCYTES
  • INFLUENCES HORMONES OF REPRODUCTIVE SYSTEM
hormones of the adrenal gland

HORMONES OF THE ADRENAL GLAND

CORTICAL VS MEDULLARY HORMONES

hormones of the adrenal medulla
HORMONES OF THE ADRENAL MEDULLA
  • EPINEPHRINE
  • NOREPINEPHRINE
  • SIMILAR TO SYMPATHETIC GANGLION
  • INNERVATED BY PREGANGLIONIC NERVE FIBERS FROM THE SYMPATHETIC NERVOUS SYSTEM
hormone secretion
HORMONE SECRETION
  • EPINEPHRINE MAKES UP 75-80 % OF SECRETION
  • NOREPINEPHRINE MAKES UP 20-25 % OF SECRETION
  • METABOLIC CHANGES REACH PEAK AT ABOUT 30 SECONDS AFTER HORMONE RELEASE
  • EFFECTS MAY LAST AS LONG AS SEVERAL MINUTES
andrenergic receptors
ANDRENERGIC RECEPTORS
  • ALPHA
  • BETA
  • ALL ARE G LINKED RECEPTORS
  • NON CHANNEL LINKED RECEPTORS
norepinephrine
NOREPINEPHRINE
  • BINDS WITH
    • ALPHA 1-- EFFECTIVELY
    • ALPHA 2 -- EFFECTIVELY
    • BETA 1-- EFFECTIVELY
    • BETA 2 --WEAKLY IF AT ALL
epinephrine
EPINEPHRINE
  • BINDS EFFECTIVELY WITH
    • ALPHA 1-- EFFECTIVELY
    • ALPHA 2 -- EFFECTIVELY
    • BETA 1-- EFFECTIVELY
    • BETA 2 --EFFECTIVELY
alpha receptors
ALPHA RECEPTORS
  • MOST COMMON ALPHA RECEPTOR
  • ACTIVATES Gp PROTEINS
  • G PROTEINS ACTIVATE ENZYMES
alpha 2 receptors
ALPHA 2 RECEPTORS
  • LESS COMMON THAN ALPHA 1
  • ACTIVATES INHIBITORY GI PROTEINS
  • REDUCE THE FORMATION OF cyclic AMP
alpha receptors1
ALPHA RECEPTORS
  • VASOCONSTRICTION
  • IRIS DILATION
  • INTESTINAL RELAXATION
  • INTESTINAL SPHINCTER CONTRACTION
  • PILOMOTOR CONTRACTION
  • BLADDER SPHINCTER CONTRACTION
beta 1 receptors
BETA 1 RECEPTORS
  • HEART AND KIDNEYS
  • ACTIVATES G PROTEINS
  • STIMULATES PRODUCTION OF cyclic AMP
beta 2 receptor
BETA 2 RECEPTOR
  • ACTIVATES STIMULATORY G PROTEINS
beta receptors
BETA RECEPTORS
  • VASODILATION
  • CARDIOACCELERATION
  • INCREASED MYOCARDIAL STRENGTH
  • INTESTINAL RELAXATION
  • UTERUS RELAXATION
  • BRONCHIOLE DILATION
  • CALORIGENESIS
  • GLYCOGENOLYSIS
  • LIPOLYSIS
  • BLADDER RELAXATION
importance of different receptors
IMPORTANCE OF DIFFERENT RECEPTORS
  • AT LEAST PARTIALLY RESPONSIBLE FOR DIFFENCE IN ACTIVITY OF EPINEPHRINE AND NOREPINEPHRINE
generalized effects of epinephrine and norepinephrine
GENERALIZED EFFECTS OF EPINEPHRINE AND NOREPINEPHRINE
  • MOBILIZATION OF GLYCOGEN
  • INCREASES CATABOLISM OF GLUCOSE
  • RESERVES IN SKELETAL MUSCLE AND LIVER
  • LIPOLYSIS AND MOBILIZATION OF FAT RESERVES
  • INCREASE IN RATE AND FORCE OF CARDIAC MUSCLE CONTRACTION
vasoconstriction due to catecholamine hormones
VASOCONSTRICTION DUE TO CATECHOLAMINE HORMONES
  • VASOCONSTRICTOR MECHANISM
  • WORKS WITH SYMPATHETIC NERVOUS SYSTEM
  • CONSTRICT MOST BLOOD VESSELS
  • CONSTRICT VEINS
  • REACH AREAS SYMPATHETIC NERVOUS SYSTEM DOES NOT
vasodilation by epinephrine
VASODILATION BY EPINEPHRINE
  • CAUSES MILD VASODILATION
  • IN SKELETAL
  • IN CARDIAC
dilation of bronchioles by catecholamine hormones
DILATION OF BRONCHIOLES BY CATECHOLAMINE HORMONES
  • SECRETED IN RESPONSE TO SYMPATHETIC INNERVATION
  • RELAX BRONCHIOLES
effect of epinephrne on glycogenolysis
EFFECT OF EPINEPHRNE ON GLYCOGENOLYSIS
  • INNERVATION
  • ACTIVATES PHOSPHORYLASE
  • IN LIVER AND IN MUSCLES
  • BREAKS DOWN GLYCOGEN TO GLUCOSE
effects of catecholamine hormones on cardiac muscle
EFFECTS OF CATECHOLAMINE HORMONES ON CARDIAC MUSCLE
  • INCREASE RATE OF SINOATRIAL NODE DISCHARGE
  • INCREASES RATE OF CONDUCTION
  • INCREASES EXCITABILITY OF HEART MUSCLE
  • INCREASES PERMEABILITY TO CALCIUM AND SODIUM
effects of catecholamine hormones on fat utilization
EFFECTS OF CATECHOLAMINE HORMONES ON FAT UTILIZATION
  • HEAVY EXERCISE BRINGS ABOUT DRAMATIC INCREASE IN FAT UTILILZATION
  • DUE TO RAPID RELEASE OF NOREPINEPHRINE AND EPINEPHRINE
  • DUE TO SYMPATHETIC INNERVATION OF ADRENAL MEDULLA
  • ACTIVATE HORMONE-SENSITIVE LIPASE
  • LYPOLYSIS AND MOBILIZATION OF FATTY ACIDS
effects of catecholamine hormones on smooth muscle
EFFECTS OF CATECHOLAMINE HORMONES ON SMOOTH MUSCLE
  • MOST HORMONES AFFECT SMOOTH MUSCLE
  • VARYING DEGREES
  • EFFECT WILL DEPEND ON TYPE OF RECEPTOR (INHIBITORY VS EXCITATORY)
the relationship between medullary hormones and the ans
THE RELATIONSHIP BETWEEN MEDULLARY HORMONES AND THE ANS
  • ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM USUALLY LEADS TO RELEASE OF CATECHOLAMINES BY ADRENAL MEDULLA
  • SYMPATHETIC NERVOUS SYSTEM AND ADRENAL MEDULLA SUPPORT ONE ANOTHER
hormones of the adrenal cortex

HORMONES OF THE ADRENAL CORTEX

MINERALOCORTICOIDS, GLUCOCORTICOIDS, & ANDROGENIC HORMONES

aldosterone
ALDOSTERONE
  • VERY POTENT
  • 95% OF MINERALOCORTICOID SECRETION
  • PRODUCED BY ZONA GLOMERULOSA
generalized effects of aldosterone secretion
GENERALIZED EFFECTS OF ALDOSTERONE SECRETION
  • STIMULATES CONSERVATION OF SODIUM IONS
  • STIMULATES ELIMINATION OF POTASSIUM IONS
  • REABSORPTION OF SODIUM IONS HAS SECODARY EFFECT OF ENHANCING OSMOTIC REABSORPTION
  • INCREASES SENSITIVITY OF TASTE BUDS IN TONGUE TO SALT
target cells of aldosterone
TARGET CELLS OF ALDOSTERONE
  • KIDNEYS
  • SWEAT GALNDS
  • SALIVARY GLANDS
  • PANCREAS
effect of aldosterone on the kidneys
EFFECT OF ALDOSTERONE ON THE KIDNEYS
  • MOST IMPORTANT FUNCTION
  • CAUSES TRANSPORT OF SODIUM AND POTASSIUM THROUGH RENAL TUBULES
  • CAUSES TRANSPORT OF HYDROGEN IONS THROUGH RENAL TUBULES
effect of aldosterone on tubular reabsorption of na and tubular secretion of k
EFFECT OF ALDOSTERONE ON TUBULAR REABSORPTION OF Na+ AND TUBULAR SECRETION OF K+
  • TUBULAR EPITHELIAL CELLS
  • EXCHANGE TRANSPORT
  • DISTAL TUBULES AND COLLECTING TUBULES
  • CONSERVES Na+ --ELIMINATES K+
effects of high concentrations of aldosterone
EFFECTS OF HIGH CONCENTRATIONS OF ALDOSTERONE
  • DECREASE SODIUM LOSS TO A FEW MILLIGRAMS PER DAY
  • GREAT INCREASE IN POTASSIUM LOSS IN URINE
effects of total lack of aldosterone
EFFECTS OF TOTAL LACK OF ALDOSTERONE
  • CAN INCREASE SODIUM LOSS UP TO 20 GRAMS PER DAY
  • POTASSIUM IS CONSERVED AND LITTLE IS LOST
effects of high aldosterone on extracellular water volume
EFFECTS OF HIGH ALDOSTERONE ON EXTRACELLULAR WATER VOLUME
  • CAN INCREASE EXTRACELLULAR FLUID VOLUME
  • UP TO 10 TO 20% OVER NORMAL
effects of aldosterone loss on extrafluid volume
EFFECTS OF ALDOSTERONE LOSS ON EXTRAFLUID VOLUME
  • CAN DECREASE EXTRACELLULAR FLUID VOLUME
  • UP TO 20 TO 25% BELOW NORMAL
effects of exessive potassium loss
EFFECTS OF EXESSIVE POTASSIUM LOSS
  • CAN CAUSE A SERIOUS DECREASE OF POTASSIUM
  • HYPOKALEMIA
effects of hypokalemia
EFFECTS OF HYPOKALEMIA
  • SEVERE MUSCLE WEAKNESS
  • MUSCLE PARALYSIS
  • DUE TO EFFECTS ON NERVE AND MUSCLE FIBER MEMBRANES
effects of hyperkalemia
EFFECTS OF HYPERKALEMIA
  • CARDIAC TOXICITY OCCURS WHEN POTASSIUM LEVELS DOUBLE
  • SYMPTOMS WEAKNESS OF CONTRACTION ARRHYTHMIAIF LEVELS RISE FURTHER CAN LEAD TO DEATH
effects of aldosterone on tubular secretion of hydrogen ions
EFFECTS OF ALDOSTERONE ON TUBULAR SECRETION OF HYDROGEN IONS
  • ALSO CAUSES HYDROGEN IONS TO BE EXCHANGED FOR SODIUM IONS
    • TO LESSER EXTENT
  • DECREASES HYDROGEN ION CONCENTRATION IN EXTRACELLULAR FLUID
  • NOT STRONG EFFECT
  • CAUSES MILD DEGREE OF ALKALOSIS
effects of aldosterone lack on the circulatory system
EFFECTS OF ALDOSTERONE LACK ON THE CIRCULATORY SYSTEM
  • CAN CAUSE A 20-25% DECREASE OF BLOOD VOLUME & EXTRACELLULAR FLUIDS CAN CAUSE CIRCULATORY SHOCK
  • WITHOUT TREATMENT MAY DIE WITH 4-8 DAYS
effect of hypersecretion of aldosterone on the circulatory system
EFFECT OF HYPERSECRETION OF ALDOSTERONE ON THE CIRCULATORY SYSTEM
  • EXTRACELLULAR FLUID VOLUME INCREASES
  • BLOOD VOLUME INCREASES
  • CARDIAC OUTPUT INCREASES
  • TO AS MUCH AS 20 TO 30% ABOVE NORMAL AT FIRST
  • COMPENSATORY MECHANISMS RETURN IT DOWN TO 5-10 %
factors that affect the regulation of aldosterone secretion
FACTORS THAT AFFECT THE REGULATION OF ALDOSTERONE SECRETION
  • POTASSIUM ION CONCENTRATION OF THE EXTRACELLULAR FLUID
  • RENIN-ANGIOTENSIN SYSTEM
  • QUANTITY OF BODY SODIUM
  • ADENOCORTICOTROPIC HORMONE
aldosterone is not as dependent on crh and acth

ALDOSTERONE IS NOT AS DEPENDENT ON CRH AND ACTH

ANGIOTENSIN AND POTASSIUM LEVELS ARE THE MAJOR REGULATORS

importance of potassium ions in aldosterone secretion
IMPORTANCE OF POTASSIUM IONS IN ALDOSTERONE SECRETION
  • INCREASE IN POTASSIUM IONS CAUSES INCREASED SECRETION OF ALDOSTERONE
  • ALDOSTERONE CAUSES ENHANCED EXCRETION OF POTASSIUM
  • POTASSIUM LEVELS RETURN TO NORMAL
renin
RENIN
  • KEY IN RENIN-ANGIOTENSIN SYSTEM
  • RELEASED BY JUXTAGLOMERULAR COMPLEX OF KIDNEYS
  • SECRETED AS PRORENIN
  • CONVERTED TO RENIN BEFORE ENTERING BLOODSTREAM
factors that increase renin secretion
FACTORS THAT INCREASE RENIN SECRETION
  • SYMPATHETIC INNERVATION
  • DECLINE IN RENAL BLOOD FLOW
effects of renin
EFFECTS OF RENIN
  • CATALYZES CONVERSION OF ANGIOTENSINOGEN TO ANGIOTENSIN I
  • ANGIOTENSIN I CONVERTED TO ANGIOTENSIN II AS PASSES THROUGH LUNGS
  • ANGIOTENSIN CONVERTING ENZYME (ACE)
effects of angiotensin ii
EFFECTS OF ANGIOTENSIN II
  • STIMULATES SECRETION OF ADH STIMULATES WATER REABSORPTION COMPLEMENTS ALDOSTERONE
  • STIMULATES SECRETION OF ALDOSTERONE BY ADRENAL GLANDS INCREASES RETENTION OF SODIUM INCREASES LOSS OF POTASSIUM
  • STIMULATES THIRST INCREASES FLUID CONSUMPTION INCREASES BLOOD VOLUME
  • INCREASES CONSTRICTION OF ARTERIOLES ELEVATES SYSTEMIC BLOOD PRESSURE
generalized effects of cortisol
GENERALIZED EFFECTS OF CORTISOL
  • CARBOHYDRATE METABOLISM
  • PROTEIN METABOLISM
  • FAT METABOLISM
  • STRESS MANAGEMENT
  • ANTI-INFLAMMATORY EFFECTS
effect of cortisol on gluconeogenesis
EFFECT OF CORTISOL ON GLUCONEOGENESIS
  • INCREASE 6 TO 10 TIMES
  • INCREASES ENZYMES NEEDED TO CONVERT AMINO ACIDS TO GLUCOSE DUE TO INCREASED TRANSCRIPTION
  • INCREASES MOBILILIZATION OF AMINO ACIDS FROM TISSUES MUSCLE MAIN SOURCE
  • INCREASES AMINO ACID CONCENTRATON IN BLOOD
effects of cortisol on glucose utilization by cells
EFFECTS OF CORTISOL ON GLUCOSE UTILIZATION BY CELLS
  • MODERATE DECREASE IN GLUCOSE USE
  • DECREASE OCCURS SOMEWHERE BETWEEN POINT OF ENTRY AND FINAL DEGRADATION
  • COULD ALSO INVOLVE TRANSPORT MECHANISMS
effects of cortisol on blood glucose concentrations
EFFECTS OF CORTISOL ON BLOOD GLUCOSE CONCENTRATIONS
  • INCREASED GLUCONEOGENESIS
  • DECREASED GLUCOSE USE
  • RAISES BLOOD GLUCOSE LEVELS
adrenal diabetes
ADRENAL DIABETES
  • INCREASE COULD BE AS LARGE AS 50 % ABOVE NORMAL
  • SIMILAR TO PITUITARY DIABETES BUT DIFFERENT FROM INSULIN DEFICIENCY
effects of cortisol on cellular proteins stores
EFFECTS OF CORTISOL ON CELLULAR PROTEINS STORES
  • REDUCES PROTEIN STORES EXCEPT IN LIVER
  • DECREASED PROTEIN SYNTHESIS
  • DECREASE IN FORMATION OF RNA
  • INCREASED CATABOLISM OF PROTEIN
  • DECREASED TRANSPORT OF AMINO ACIDS INTO TISSUES OTHER THAN LIVER
effects of cortisol on the liver and plasma protein concentrations
EFFECTS OF CORTISOL ON THE LIVER AND PLASMA PROTEIN CONCENTRATIONS
  • SYNTHESIS OF PROTEINS IN LIVER INCREASES
    • INCREASED ACTIVITY OF LIVER ENZYMES
  • PLASMA PROTEINS PRODUCED ARE RELEASED INTO BLOOD
slide157
EFFECTS OF CORTISOL ON MOVEMENTS OF AMINO ACIDS INTO AND OUT OF THE BLOOD AND BLOOD AMINO ACID CONCENTRATIONS
  • DEPRESSES UPTAKE BY MUSCLE AND OTHER CELLS
  • INCREASED UPTAKE BY LIVER
  • INCREASES PLASMA CONCENTRATIONS OF AMINO ACIDS
effects of increased plasma concentrations of amino acids on liver utilization of amino acids
EFFECTS OF INCREASED PLASMA CONCENTRATIONS OF AMINO ACIDS ON LIVER UTILIZATION OF AMINO ACIDS
  • INCREASED DEAMINATION OF AMINO ACIDS
  • INCREASED PROTEIN SYNTHESIS
  • INCREASED SYNTHESIS OF PLASMA PROTEINS
  • INCREASED GLUCONEOGENESIS
effect of cortisol on the mobilization of fats
EFFECT OF CORTISOL ON THE MOBILIZATION OF FATS
  • INCREASES MOBILIZATION OF FATTY ACIDS FROM ADIPOSE TISSUE
  • INCREASES PLASMA FATTY ACID CONCENTRATIONS
  • MODERATELY INCREASES OXIDATION OF FATTY ACIDS
  • SHIFTS BODY TO FAT METABOLISM IN STARVATION OR STRESS
  • EFFECT DEVELOPS OVER SEVERAL HOURS
  • GLYCOGEN AND GLUCOSE SPARER
effects of cortisol in stressful situation
EFFECTS OF CORTISOL IN STRESSFUL SITUATION
  • ANY KIND OF STRESS INCREASES ACTH SECRETION
  • INCREASED SECRETIONS OF CORTISOL IN MINUTES
effects of cortisol on the inflammatory response
EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
  • INFLAMMATION IS TRIGGERED BY TRAUMA, INFECTION OR A VARIETY OF OTHER MECHANISMS
  • CORTISOL CAN BLOCK INFLAMMATION
  • CAN EVEN REVERSE MANY OF ITS EFFECTS
specific effects of cortisol on the inflammatory response
SPECIFIC EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
  • STABILIZES LYSOSOMAL MEMBRANES
  • BLOCKS MOST OF THE FACTORS CAUSING INFLAMMATION
  • INCREASES HEALING PROCESS
importance of cortisol in fighting disease
IMPORTANCE OF CORTISOL IN FIGHTING DISEASE
  • RHEUMATOID ARTHRITIS
  • RHEUMATIC FEVER
  • ACUTE GLOMERULONEPHRITIS
control of cortisol secretion
CONTROL OF CORTISOL SECRETION
  • ACTH IS THE MAJOR FACTOR CAUSING CORTISOL SECRETION
effect of corticotropin releasing hormone in acth secretion
EFFECT OF CORTICOTROPIN RELEASING HORMONE IN ACTH SECRETION
  • SMALL PEPTIDE FROM HYPOTHALAMUS
  • LITTLE ACTH IS SECRETED IN THE ABSENCE OF CRH
effects of physiological stress on acth secretion
EFFECTS OF PHYSIOLOGICAL STRESS ON ACTH SECRETION
  • CAN LEAD TO INCREASE ACTH
  • CAN RESULT IN INCREASED LEVELS OF CORTISOL WITHIN A FEW MINUTES
  • REGULATED BY HYPOTHALAMUS AND THE RELEASE OF CRH
feedback controls on acth secretion
FEEDBACK CONTROLS ON ACTH SECRETION
  • CORTISOL HAS A DIRECT NEGATIVE FEEDBACK EFFECT
    • ON HYPOTHALAMUS DECREASING CRH
    • ON ANTERIOR PITUITARY DECREASING ACTH
pancreatic hormones
PANCREATIC HORMONES
  • GLUCAGON
  • INSULIN
  • SOMATOSTATIN
  • PANCREATIC POLYPEPTIDE
somatostatin
SOMATOSTATIN
  • PRODUCED BY DELTA CELLS
  • IDENTICAL TO BRAIN FORM
  • SUPPRESSES RELEASE OF GLUCAGON AND INSULIN
  • SLOWS RATE OF FOOD ABSORPTION
  • SLOWS RATE OF ENZYME SECRETION
pancreatic polypeptide
PANCREATIC POLYPEPTIDE
  • INHIBITS GALLBLADDER CONTRACTIONS
  • REGULATES PRODUCTION OF SOME PANCREATIC ENZYMES
  • MAY HELP IN CONTOLLING RATE OF ABSORPTION IN GI TRACT
insulin
INSULIN
  • POLYPEPTIDE HORMONE
  • SECRETED BY BETA CELLS
  • WHEN GLUCOSE LEVELS RISE ABOVE NORMAL LEVELSOR
  • WHEN ELEVATED LEVELS OF ARGININE, LEUCINE AND OTHER HORMONES ARE PRESENT IN THE BLOOD
insulin dependent cells
INSULIN DEPENDENT CELLS
  • MOST ALL THE CELL IN BODY
insulin independent cells
INSULIN INDEPENDENT CELLS
  • BRAIN
  • KIDNEYS
  • LINING OF GI TRACT
  • RED BLOOD CELLS
generalized effects of insulin
GENERALIZED EFFECTS OF INSULIN
  • ACCELERATION OF GLUCOSE UPTAKE IN ALL TARGET CELLS
  • ACCELERATION OF GLUCOSE UTILIZATION IN ALL TARGET CELLS
  • ENHANCED ATP PRODUCTION IN ALL TARGET CELLS
  • STIMULATION OF GLYCOGENESIS IN SKELETAL AND LIVER CELLS
  • STIMULATION OF AMINO ACID ABSORPTION IN ALL TARGET TISSUES
  • STIMULATION OF PROTEIN SYNTHESIS IN ALL TARGET TISSUES
  • STIMULATION OF LIPOGENESIS IN ALL TARGET TISSUES
effects of insulin on carbohydrate metabolism
EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM
  • RAPID UPTAKE OF GLUCOSE
  • STORAGE OF GLUCOSE AS GLYCOGEN
  • CATABOLISM OF GLUCOSE
  • ESPECIALLY IN ADIPOSE, LIVER AND SKELETAL TISSUES
effects of insulin on the uptake storage and use of glucose by the liver
EFFECTS OF INSULIN ON THE UPTAKE, STORAGE AND USE OF GLUCOSE BY THE LIVER
  • MOST OF GLUCOSE ABSORBED AFTER MEAL IS STORED IN LIVER AS GLYCOGEN
  • ACTS AS A RESERVE TO SUPPLY GLUCOSE BETWEEN MEALS
mechanisms of glucose uptake
MECHANISMS OF GLUCOSE UPTAKE
  • INSULIN INHIBITS PHOSPHORYLASE
  • ENHANCES UPTAKE OF GLUCOSE BY HEPATOCYTES
    • INCREASES ACTIVITY OF GLUCOKINASE
      • ENZYME PHOSPHORYLATES GLUCOSE TRAPPING IT INSIDE CELL
  • INCREASES ACTIVITY OF ENZYMES PROMOTING GLYCOGENESIS
  • NET EFFECT IS TO INCREASE GLYOGEN LEVELS IN LIVER
glycogen storage in liver
GLYCOGEN STORAGE IN LIVER
  • ABOUT 5-6 PERCENT OF LIVER MASS
  • USUALLY 100 GRAMS
other effects of insulin on carbohydrate metabolism in the liver
OTHER EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM IN THE LIVER
  • PROMOTES CONVERSION OF LIVER GLUCOSE INTO FATTY ACIDS
  • FATTY ACIDS ARE THEN TRANSPORTED TO ADIPOSE TISSUES AND DEPOSITED
  • INHIBITS GLUCONEOGENESIS
    • DECREASES ACTIVITIES OF ENZYMES
effects of insulin on glucose metabolism in muscle cells
EFFECTS OF INSULIN ON GLUCOSE METABOLISM IN MUSCLE CELLS
  • MUSCLES GENERALLY USE FATTY ACIDS AS THEIR ENERGY SOURCE
  • RESTING MEMBRANE IS ALMOST IMPERMEABLE TO GLUCOSE
  • UNTIL STIMULATED BY INSULIN
conditions where muscles use considerable glucose
CONDITIONS WHERE MUSCLES USE CONSIDERABLE GLUCOSE
  • DURING PERIODS OF HEAVY EXERCISE
  • DURING THE FIRST FEW HOURS AFTER A MEAL WHEN INSULIN LEVELS ARE HIGH
effects of heavy exercise on muscle cells
EFFECTS OF HEAVY EXERCISE ON MUSCLE CELLS
  • DOES NOT REQUIRE LARGE AMOUNTS OF INSULIN
  • MEMBRANE PERMEABILITY CHANGES DUE TO CONTRACTILE PROCESS
effects of insulin
EFFECTS OF INSULIN
  • CAUSES RAPID TRANSPORT OF GLUCOSE INTO THE CELLS
effect of insulin on the storage of glycogen in muscle cells
EFFECT OF INSULIN ON THE STORAGE OF GLYCOGEN IN MUSCLE CELLS
  • IN RESTING MUSCLES AFTER MEAL
  • GLUCOSE IS STORED AS MUSCLE GLYCOGEN
  • CONCENTRATION CAN BE AS MUCH AS 1-2 % OF CELL MASS
  • CAN BE USED AS ENERGY RESERVE
differences between liver glycogen and muscle glycogen
DIFFERENCES BETWEEN LIVER GLYCOGEN AND MUSCLE GLYCOGEN
  • MUSCLE GLYCOGEN CANNOT BE RECONVERTED TO GLUCOSE AND RELEASED INTO BLOOD STREAM WHILE LIVER CELLS CAN
  • MUSCLE CELLS DO NOT HAVE GLUCOSE PHOSPHATASE
  • LIVER CELLS HAVE GLUCOSE PHOSPHATASE
mechanism by which insulin increases glucose transport in muscle cells
MECHANISM BY WHICH INSULIN INCREASES GLUCOSE TRANSPORT IN MUSCLE CELLS
  • SOME GLUCOSE TRAPPING BY GLUCOKINASE
  • ENHANCES FACILITATED DIFFUSION OF GLUCOSE THROUGH MEMBRANE
  • TAKES ONLY A FEW SECONDS
effects of glucose on the brain
EFFECTS OF GLUCOSE ON THE BRAIN
  • INSULIN INDEPENDENT
  • PERMEABLE TO GLUCOSE WITH OR WITHOUT INSULIN
  • BRAIN DEPENDENT ON GLUCOSE
blood glucose levels are maintained due to the brains need for glucose
BLOOD GLUCOSE LEVELS ARE MAINTAINED DUE TO THE BRAINS NEED FOR GLUCOSE
  • BLOOD GLUCOSE LEVELS MUST ALWAYS MAINTAIN A CRITICAL LEVEL
  • LEVELS IN A RANGE OF 20-50 mg/100 ml CAUSES HYPOGLYCEMIC SHOCK
symptoms of hypoglycemic shock
SYMPTOMS OF HYPOGLYCEMIC SHOCK
  • PROGESSIVE IRRITABILITY
  • FAINTING
  • CONVULSIONS
  • COMA
  • DEATH
effect of insulin on fat metabolism
EFFECT OF INSULIN ON FAT METABOLISM
  • MAY NOT BE AS DRAMATIC AS CARBOHYDRATE
  • BUT IS MORE IMPORTANT
  • INSULIN IS A PROTEIN SPARER
  • EFFECTS OF INSULIN ARE BEST SEEN WHEN THERE IS A LACK OF INSULIN
effects of insulin on excess fat synthesis and storage
EFFECTS OF INSULIN ON EXCESS FAT SYNTHESIS AND STORAGE
  • SEVERAL EFFECTS LEAD TO AN INCREASE IN FAT STORAGE
  • INCREASE IN GLUCOSE UTILIZATION BY MANY OF BODY’S CELLS
  • INSULIN ALSO PROMOTES FATTYACID SYNTHESIS IN LIVER
  • INSULIN PROMOTES A SMALL AMOUNT OF FATTY ACID SYNTHESIS IN THE ADIPOSE CELLS
factors that lead to an increase in fatty acid synthesis in the liver
FACTORS THAT LEAD TO AN INCREASE IN FATTY ACID SYNTHESIS IN THE LIVER
  • INCREASED TRANSPORT OF GLUCOSE INTO HEPATOCYTES
  • EXCESS CITRATE AND ISOCITRATE IONS ARE FORMED BY CITRIC ACID CYCLE
  • TRANSPORT OF FATTY ACIDS TO THE ADIPOSE TISSUES
increased transport of glucose into the liver
INCREASED TRANSPORT OF GLUCOSE INTO THE LIVER
  • PHOSPHORYLATION
  • CONVERSION OF GLUCOSE TO PYRUVATE
  • CONVERSION OF PYRUVATE TO ACETYL-coA
  • SYTHESIS OF FATTY ACIDS FROM ACETYL coA
excess citrate and isocitrate ions from the citric acid cycle
EXCESS CITRATE AND ISOCITRATE IONS FROM THE CITRIC ACID CYCLE
  • FORMED WHEN EXCESSIVE AMOUNTS OF GLUCOSE ARE BEING USED FOR ENERGY
  • DIRECTLY ACTIVATE ACETYL-coA CARBOXYLASE
    • CATALYZES FIRST STAGE OF FATTY ACID SYNTHESIS
fatty acids are then transported to the adipose tissues
FATTY ACIDS ARE THEN TRANSPORTED TO THE ADIPOSE TISSUES
  • REMOVES THEM AND PREVENTS A NEGATIVE FEEDBACK EFFECT ON ACETYL-co CARBOXYLASE
effects of insulin of fat storage at the adipose tissues
EFFECTS OF INSULIN OF FAT STORAGE AT THE ADIPOSE TISSUES
  • SAME EFFECT AS IN THE LIVER BUT SMALLER
  • ONE TENTH AS MUCH GLUCOSE IS TRANSPORTED INTO ADIPOSE CELLS
essential effects of insulin on fat storage in the adipose tissues
ESSENTIAL EFFECTS OF INSULIN ON FAT STORAGE IN THE ADIPOSE TISSUES
  • INHIBITS THE ACTIVITY OF HORMONE SENSITVE LIPASE
    • CATALYZES LIPOLYSIS
  • PROMOTES TRANSPORT OF GLUCOSE INTO CELLS SAME AS IN MUSCLE CELLS USED TO FORM GLYCEROL
effects of insulin on protein metabolsism
EFFECTS OF INSULIN ON PROTEIN METABOLSISM
  • WITH GH PROMOTES UPTAKE OF AMINO ACIDS INTO CELLS
  • DIRECTLY AFFECTS RIBOSOME TO CAUSE TRANSLATION
  • INCREASES (OVER TIME) TRANSCRIPTION
  • INHIIBITS CATABOLISM OF PROTEINS
  • INHIBITS GLUCONEOGENESIS ENZYMES IN LIVER
effect of insulin on growth
EFFECT OF INSULIN ON GROWTH
  • INSULIN WORKS WITH GROWTH HORMONE
    • SYNERGISTIC EFFECT
  • ANIMALS DEPRIVED OF EITHER PITUITARY OR PANCREAS DISPLAY STUNTED GROWTH
  • BOTH NEED TO BE PROVIDED FOR NORMAL GROWTH
control of insulin secretion
CONTROL OF INSULIN SECRETION
  • BY BLOOD GLUCOSE LEVELS IN THE BLOOD
  • BY AMINO ACID LEVELS IN THE BLOOD
  • BY GASTROINTESTINAL HORMONES
effects of blood glucose levels on insulin secretion
EFFECTS OF BLOOD GLUCOSE LEVELS ON INSULIN SECRETION
  • 80-90 mg/100ML--MINIMAL INSULIN SECRETION
  • ABOVE 100mg/100ML --INSULIN SECRETION RISES QUICKLY
  • CAN REACH AS MUCH AS 400 - 600 mg/100ML
  • SECRETION DECREASES RAPIDLY AS BLOOD GLUCOSE LEVELS RETURN TO FASTING LEVEL
effect of amino acids on insulin secretion
EFFECT OF AMINO ACIDS ON INSULIN SECRETION
  • SOME OF THE AMINO ACIDS CAUSE INCREASED SECRETION
    • IE ARGININE AND LEUCINE
  • AMINO ACIDS ADMINISTERED WITHOUT AN ACCOMPANYING RISE IN BLOOD GLUCOSE WILL CAUSE ONLY A SMALL RISE IN SECRETION
  • IF BOTH ARE PRESENT INSULIN SECRETION MAY BE DOUBLED
effect of gastrointestinal hormones on insulin secretion
EFFECT OF GASTROINTESTINAL HORMONES ON INSULIN SECRETION
  • GASTRIN
  • SECRETIN
  • CCK
  • GASTRIC INHIBITORY PEPTIDE
  • RELEASED AFTER EATING
  • SEEM TO CAUSE AN ANTICIPITORY RISE IN INSULIN SECRETION
  • ALMOST DOUBLE SECRETION OF INSULIN AFTER A MEAL
carbohydrate vs fatty acid lipid metabolism

CARBOHYDRATE VS FATTY ACID (LIPID) METABOLISM

INSULIN DETERMINES WHICH WILL OCCUR

glucagon
GLUCAGON
  • PRODUCED BY ALPHA CELLS
generalized effects of glucagon
GENERALIZED EFFECTS OF GLUCAGON
  • GLYCOGENOLYSIS IN SKELETAL AND LIVER CELLS
  • LIPOLYSIS AND FATTY ACID MOBILIZATION IN ADIPOSE TISSUES
  • GLUCONEOGENESIS AT THE LIVER
  • REDUCTION OF GLUCOSE UTILIZATION
  • INCREASE IN BLOOD GLUCOSE LEVELS
glycogenolysis and increased blood glucose levels caused by glucagon
GLYCOGENOLYSIS AND INCREASED BLOOD GLUCOSE LEVELS CAUSED BY GLUCAGON
  • MOST DRAMATIC EFFECT
  • INCREASES BLOOD GLUCOSE LEVELS IN MINUTES
mechanisms of activating glycogenolysis in the liver
MECHANISMS OF ACTIVATING GLYCOGENOLYSIS IN THE LIVER
  • ACTIVATES ADENYLATE CYCLASE
  • FORMS c AMP
  • ACTIVATES PROTEIN KINASE REGULATOR PROTEIN
  • ACTIVATES PROTEIN KINASE
  • ACTIVATES PHOSPHORYLASE b KINASE
  • CONVERTS PHOSPHORYLASE b INTO PHOSPHORYLASE a
  • PROMOTES THE PHOSPHORLYSIS OF GLYCOGEN INTO GLUCOSE 1 PHOSPHATE
  • GLUCOSE 1 PHOSPHATE IS DEPHOSPHORYLATED AND LEAVES THE HEPATOCYTE BY FACILITATED DIFFUSION
effect of glucagon on gluconeogenesis in the liver
EFFECT OF GLUCAGON ON GLUCONEOGENESIS IN THE LIVER
  • NONCARBOHYDRATE SUBSTRATES ARE CONVERTED TO PYRUVATE OR AN INTERMEDIATE IN THE CITRIC ACID CYCLE
  • AMINO ACIDS ARE CONVERTED TO PYRUVATE OR PHOSPHOPHENOLPYRUVATE
  • LIPIDS CAN BE CONVERTED TO PGA, PGAL OR ANOTHER 3 CARBON INTERMEDIATE
  • GLUCONEOGENESIS HAS SAME INTERMEDIATES AS GLYCOLYSIS
  • BUT ITS ENZYMES RUN IT FROM PYRUVATE TO GLUCOSE
regulation of glucagon secretion
REGULATION OF GLUCAGON SECRETION
  • BLOOD GLUCOSE CONCENTRATIONS
  • OPPOSITE EFFECT THAN IT HAS ON INSULIN
  • WHEN BLOOD GLUCOSE FALLS AS LOW AS 70mg/100ML LARGE AMOUNTS OF GLUCAGON ARE SECRETED
  • PROTECTS THE BODY AGAINST HYPOGLYCEMIA
effects of amino acids on glucagon secretion
EFFECTS OF AMINO ACIDS ON GLUCAGON SECRETION
  • HELPS PREVENT HYPOGLYCEMIA THAT WOULD OCCUR IF YOU ATE A MEAL OF PURE PROTEIN
in normal individual
IN NORMAL INDIVIDUAL
  • BLOOD GLUCOSE LEVELS ARE TIGHTLY REGULATED
  • BETWEEN 80-90 IN THE MORNING
  • 120 TO 140 AFTER BREAKFAST
  • RETURN TO NORMAL IN ABOUT 2 HOURS AFTER MEAL
maintenance of blood glucoses between meals
MAINTENANCE OF BLOOD GLUCOSES BETWEEN MEALS
  • LIVER ACTS AS A BLOOD GLUCOSE BUFFER
    • STORES GLUCOSE AFTER MEALS
      • AS MUCH AS 2/3 OF GLUCOSE ABSORBED IS STORED IN LIVER AS GLYCOGEN
    • RELEASES GLUCOSE BETWEEN MEAL
  • INSULIN AND GLUCAGON FUNCTION AS SEPARATE CONTROL SYSTEMS
  • IN HYPOGLYCEMIA SYMPATHETIC INNERVATION INCREASES AND STIMULATES RELEASE OF EPINEPHRINE WHICH INCREASES GLUCOSE RELEASE
  • OVER HOURS OR DAYS--GH AND CORTISOL ARE RELEASED
    • DECREASE GLUCOSE UTILIZATION
they do it all for the brain

THEY DO IT ALL FOR THE BRAIN

ALSO THE RETINA, GERMINAL EPITHELIA OF GONADS, KIDNEYS, AND OTHER INSULIN INDEPENDENT CELLS

pineal gland
PINEAL GLAND
  • PEA SIZED
  • EPITHALAMUS
  • ROOF OF DIENCEPHALON
  • NEUROENDOCRINE TRANSDUCER
neuroendocrine transducer
NEUROENDOCRINE TRANSDUCER
  • CONVERTS SIGNALS RECEIVED THROUGH NERVOUS SYSTEM INTO AN ENDOCRINE SIGNAL
relationship to hypothalamus
RELATIONSHIP TO HYPOTHALAMUS
  • INFORMATION ABOUT LIGHT AND DARK CYCLES CARRIED FROM EYES TO HYPOTHALAMUS
  • SYMPATHETIC NERVES CARRY ACTION POTENTIALS TO PINEAL GLAND
hormones of the pineal gland
HORMONES OF THE PINEAL GLAND
  • MELATONIN
  • OTHERS HAVE BEEN FOUND BUT THEY DO NOT KNOW THEIR FUNCTIONS ARGININE VASOTOCIN
melatonin
MELATONIN
  • DERIVED FROM SERATONIN
  • PRODUCTION LOWEST IN DAYLIGHT
  • PRODUCTION HIGHEST AT NIGHT
effects of melatonin
EFFECTS OF MELATONIN
  • SLOWS MATURATION OF SPERM, EGGS AND REPRODUCTIVE ORGANS REDUCES RATE OF GnRH SECRETION
  • EFFECTIVE ANTIOXIDANT
  • MAY BE INVOLVED IN CIRCADIAN RHYTHM
  • INCREASED SECRETION MAY CAUSE SEASONAL AFFECTIVE DISORDER
hormones of the reproductive tissues
HORMONES OF THE REPRODUCTIVE TISSUES
  • MALE
  • FEMALE
  • REGULATED BY FSH AND LH
the hormones of the testes
THE HORMONES OF THE TESTES
  • TESTOSTERONE
  • INHIBIN
hormones of the ovaries
HORMONES OF THE OVARIES
  • ESTROGENS ESTRADIOL, ESTRIN ESTRONE
  • PROGESTINS PROGESTERONE
  • INHIBIN
  • RELAXIN
hormones of the placenta
HORMONES OF THE PLACENTA
  • TEMPORARY ORGAN
  • ESTROGEN
  • PROGESTERONE
  • HUMAN CHORIONIC GONADOTROPIN
hormones of pregnancy
HORMONES OF PREGNANCY
  • HUMAN CHORIONIC GONADOTROPIN
  • SECRETION OF PROGESTERONE
  • SECRETION OF ESTROGEN
  • HUMAN CHORIONIC SOMATOMAMMOTROPIN
human chorionic gonadotropin
HUMAN CHORIONIC GONADOTROPIN
  • HAS STRUCTURE SIMILAR TO LUTEINIZING HORMONE
  • FIRST SECRETED BY TROPHOBLAST CELLS OF BLASTOCYST
    • BEFORE IMPLANTATION
  • SECRETED BY PLACENTA ONCE ESTABLISHED
diffuses from fetal blood into maternal blood
DIFFUSES FROM FETAL BLOOD INTO MATERNAL BLOOD
  • STIMULATES CORPUS LUTEUM
    • PREVENTS DEGENERATION
    • PREVENTS INVOLUTION
    • CAUSES IT TO ALMOST DOUBLE IN SIZE
  • STIMULATES CONTINUED SECRETION OF PROGESTERONE
    • MAINTAINS ENDOMETRIUM
  • LATER IN PREGNANCY STIMULATES SECRETION OF PROGESTERONE AND ESTROGEN
  • IMPORTANT IN MAINTAINING PREGNANCY IN FIRST 7-10 WEEKS
placenta takes over secretory function at second month
PLACENTA TAKES OVER SECRETORY FUNCTION AT SECOND MONTH
  • SECRETES ESTROGEN AND PROGESTERONE
  • PLACENTA STOPS SECRETING HUMAN CHORIONIC
    • CAUSING THE CORPUS LUTEUM TO DEGENERATE AND INVOLUTE
importance of human chorionic gonadotropin
IMPORTANCE OF HUMAN CHORIONIC GONADOTROPIN
  • PREVENTS DEGENERATION OF THE CORPUS LUTEUM
  • STIMULATES THE CORPUS LUTEUM TO SECRETE ESTROGEN
  • STIMULATES THE CORPUS LUTEUM TO SECRETE PROGESTERONE
  • STIMULATES SECRETION OF STEROIDS FROM ADRENAL CORTEX OF FETUS
  • STIMULATES FETAL GONADS TO SECRETE
  • SUPRESSES MATERNAL LYMPHOCYTES REDUCING REJECTION OF THE FETUS
progesterone secretion by the placenta
PROGESTERONE SECRETION BY THE PLACENTA
  • BEGINS SECRETION ABOUT THE 6TH WEEK OF PREGNANCY
  • THIS TOTALLY REPLACES PROGESTERONE FROM THE CORPUS LUTEUM BY THE 12TH -14TH WEEKS
role of placental progesterone
ROLE OF PLACENTAL PROGESTERONE
  • MAINTENANCE OF PREGNANCY
  • STIMULATES GROWTH OF ENDOMETRIUM
  • STIMULATES SECRETION OF NUTRIENTS ENDOMETRIAL GLANDS
  • INHIBITS CONTRACTION OF THE UTERUS
  • PREVENTS PREMATURE EXPULSION OF FETUS
  • WORKS WITH PROLACTIN & OXYTOCIN TO STIMULATE PREPARATIONS FOR LACTATION IN BREAST
  • SERVES AS A PRECURSOR FOR PLACENTAL ESTROGEN
placental estrogen
PLACENTAL ESTROGEN
  • CORPUS LUTEUM SECRETES ESTROGEN FOR FIRST MONTH
  • IN RESPONSE TO HUMAN CHORIONIC GONADOTROPIN
  • AFTER 1ST MONTH HUMAN CHORIONIC GONADOTROPIN STIMULATES ESTROGEN SECRETION FROM PLACENTA
  • LEVELS INCREASE UNTIL DELIVERY
estrogen functions
ESTROGEN FUNCTIONS
  • STIMULATES ENLARGEMENT OF THE UTERUS
  • STIMULATES BREAST GROWTH
  • STIMULATES DEVELOPMENT OF DUCTS IN BREAST
  • STIMULATES ENLARGEMENT OF GENITILIA
  • STIMULATES RELAXATION OF PELVIC LIGAMENTS
importance of the fetus in secreting placental estrogen
IMPORTANCE OF THE FETUS IN SECRETING PLACENTAL ESTROGEN
  • PLACENTA LACKS ENZYME IN ESTROGEN PATHWAY
  • FETAL ADRENAL CORTEX CONTAINS THE ENZYME NECESSARY TO CONVERT PREGNELONE TO DHEA
  • TRANSPORTED BACK TO PLACENTA AND IS CONVERTED INTO ESTRODIOL AND RELEASED
human chorionic somatomammotropin
HUMAN CHORIONIC SOMATOMAMMOTROPIN
  • SECRETION BEGINS AT ABOUT 4TH WEEK
  • RISES THROUGHOUT PREGNANCY
  • SIMILAR TO HUMAN GROWTH HORMONE
  • WEAKLY STIMULATES FETAL DEVELOPMENT AND BREAST DEVELOPMENT
  • ANTAGONISTIC TO INSULIN
    • DECREASING MATERNAL USE OF GLUCOSE
    • MAKES MORE GLUCOSE AVAILABLE TO FETUS
    • CAN CAUSE GESTATIONAL DIABETES IN MOTHER
    • PROMOTES MOBILIZATION OF FATS
hormonal changes in pregnancy
HORMONAL CHANGES IN PREGNANCY
  • INHIBITION OF GONADOTROPIN
  • STIMULATION OF PROLACTIN
  • STIMULATION OFRELAXIN
  • STIMULATION OF INSULIN
  • STIMULATION OF ALDOSTERONE
  • STIMULATION OF CORTISOL
  • STIMULATION OF THYROID HORMONE
inhibition of gonadotropins
INHIBITION OF GONADOTROPINS
  • HIGH LEVELS OF ESTROGEN AND PROGESTERONE IN BLOOD STREAM INHIBIT SECRETION OF GONADOTROPIN RELEASING HORMONE
  • THIS INHIBITS THE RELEASE OF FOLLICLE STIMULATING HORMONE AND LUTEINIZING HORMONE
  • THIS PREVENTS OVULATON AND/OR MENSTRUATION
stimulation of prolactin
STIMULATION OF PROLACTIN
  • SECRETION INCREASES THROUGHOUT PREGNANCY
  • WORKS WITH ESTROGEN AND PROGESTERONE TO STIMULATE BREAST DEVELOPMENT AND MILK PRODUCTION
stimulation of relaxin
STIMULATION OF RELAXIN
  • HUMAN CHORIONIC GONADOTROPIN STIMULATES RELAXIN SECRETION BY CORPUS LUTEUM IN FIRST TWO MONTHS
  • LATER RELAXIN IS SECRETED BY THE ENDOMETRIUM
function of relaxin
FUNCTION OF RELAXIN
  • RELAXES PELVIC LIGAMENTS
  • WORKS WITH PROGESTERONE TO INHIBIT UTERINE CONTRACTIONS
stimulation of insulin
STIMULATION OF INSULIN
  • DECREASED MATERNAL SENSITIVITY TO INSULIN CAUSES ITS SECRETION TO INCREASE
    • AFTER 3RD MONTH
  • CAN BECOME SEVERE ENOUGH TO CAUSE GESTATIONAL DIABETES
  • NORMALLY RETURNS TO NORMAL AFTER BIRTH
stimulation of aldosterone
STIMULATION OF ALDOSTERONE
  • ESTROGEN AND PROGESTERONE DIRECTLY INCREASE THE SECRETION OF ANGIOTENSIN II AND ALDOSTERONE FROM ADRENAL CORTEX
    • PROMOTE SODIUM AND WATER RETENTION
    • HELPS TO PROVIDE SODIUM TO FETUS
    • ESTROGEN SEEMS TO INHIBIT THE VASCULAR EFFECTS OF HIGH LEVELS OF ANGIOTENSIN II
stimulation of cortisol
STIMULATION OF CORTISOL
  • INCREASES IN CORTISOL SECRETION AND SECRETION OF CORTISOL BINDING GLOBULIN
    • IN RESPONSE TO STIMULATION OF ESTROGEN
    • LEAD TO AN INCREASE IN BOTH FREE AND PROTEIN BOUND CORTISOL
effects of increased cortisol levels
EFFECTS OF INCREASED CORTISOL LEVELS
  • INCREASED BODY FAT
  • DEVELOPMENT OF MAMMARY GLANDS
  • INCREASED APPETITE
  • INCREASED BLOOD GLUCOSE LEVELS
  • INCREASED GLUCOSE LEVELS INCREASE INSULIN SECRETION
  • INCREASED INSULIN SECRETION INCREASES LIPID STORAGE
increased thyroid hormone
INCREASED THYROID HORMONE
  • HIGH LEVELS OF ESTROGEN STIMULATE THYROTROPIN RELEASING HORMONE
  • STIMULATES THYROID STIMULATING HORMONE
  • RESULTS IN INCREASE IN GLAND SIZE, SECRETORY RATE, BASAL METABOLIC RATE, CARDIAC AND PULMONARY FUNCTION
the endocrine function of the heart
THE ENDOCRINE FUNCTION OF THE HEART
  • ATRIOPEPTIN/ATRIAL NATRIURETIC PEPTIDE
  • PRODUCED BY ATRIA CARDIAC MUSCLES
effects of atrial natriuretic peptide
EFFECTS OF ATRIAL NATRIURETIC PEPTIDE
  • PROMOTES LOSS OF SODIUM IONS AND WATER AT KIDNEYS
  • INHIBITS RENIN RELEASE
  • INHIBITS SECRETION OF ADH AND ALDOSTERONE
  • SUPPRESSES THIRST
  • BLOCKS ACTION OF ANGIOTENSIN II AND NOREPINEPHRINE ON ARTERIOLES
hormones of the digestive system
HORMONES OF THE DIGESTIVE SYSTEM
  • GASTRIN
  • SECRETIN
  • CHOLECYSTOKININ
gastrin
GASTRIN
  • POLYPEPTIDE
  • SECRETED BY MUCOSAL LINING
  • STIMULATES PRODUCTION OF HCL AND PEPSIN
secretin
SECRETIN
  • POLYPEPTIDE
  • FIRST HORMONE
  • SECRETED BY THE MUCOSA OF THE DUODENUM
  • STIMULATES A BICARBONATE RICH SECRETION FROM THE PANCREAS
  • CAN INHIBIT GASTRIC SECRETIONS UNDER CERTAIN CONDITIONS
  • STIMULATES SECRETION OF BILE
cholecystokinin
CHOLECYSTOKININ
  • SECRETED BY WALL OF DUODENUM
  • STIMULATES CONTRACTION OF DUODENUM
  • INHIBITS GASTRIC ACID SECRETIONS UNDER CERTAIN CONDITIONS
  • STIMULATES THE RELEASE OF ENZYMES FROM THE PANCREAS
calcitriol
CALCITRIOL
  • STEROID HORMONE
  • SECRETED IN RESPONSE TO PTH
  • DEPENDENT ON CHOLECALCIFEROL FROM SKIN OR DIET CARRIED BY TRANSCALCIFERIN
  • VITAMIN D REFERS TO ALL FORMS OF THE VITAMINS
effect of calcitriol
EFFECT OF CALCITRIOL
  • STIMULATION OF CALCIUM AND PHOSPHATE ABSORPTION BY GI TRACT
  • STIMULATE FORMATION AND DIFFERENTIATION OF OSTEOPROGENITOR CELLS AND OSTEOCLASTS
  • STIMULATING CALCUM REABSORPTION AT THE KIDNEYS
  • SUPPRESSES PARATHYROID HORMONE SECRETION
erythropoietin
ERYTHROPOIETIN
  • PEPTIDE HORMONE
  • RELEASED BY KIDNEY IN RESPONSE TO HYPOXIA IN KIDNEY TISSUES
possible causes of hypoxia
POSSIBLE CAUSES OF HYPOXIA
  • REDUCTION IN RENAL BLOOD FLOW
  • REDUCTION IN NUMBER OF RED BLOOD CELLS
  • REDUCTION IN ABILITY OF RED BLOOD CELLS TO CARRY OXYGEN
  • REDUCTION IN OXYGEN CONTENT OF AIR
  • PROBLEMS WITH THE RESPIRATORY MEMBRANE
effect of erythropoietin
EFFECT OF ERYTHROPOIETIN
  • STIMULATES HEMATOPOIESIS
  • ELEVATES BLOOD VOLUME SLIGHTLY DUE TO INCREASE IN RED BLOOD CELLS
  • IMPROVES OXYGEN DELIVERY TO PERIPHERAL TISSUES
leptin

LEPTIN

A NEW HORMONE

effects of aging
EFFECTS OF AGING
  • FEW FUNCTIONAL CHANGES
  • DECLINE IN LEVELS OF REPRODUCTIVE HORMONES
  • ENDOCRINE TISSUES MAY BECOME LESS RESPONSIVE
  • SOME TARGET CELLS IN TISSUES MAY BECOME LESS RESPONSIVE
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