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Chapter 14: The Kidneys and Regulation of Water and Inorganic Ions. Section A: Basic Principles of Renal Physiology : 1- Glomerular filtration 2- Tubular reabsorption 3- Tubular secretion. Figure 14-1.

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Presentation Transcript
slide3

Section A:

Basic Principles of Renal Physiology:

1- Glomerular filtration

2- Tubular reabsorption

3- Tubular secretion

slide5

Figure 14-1

The paired kidneys form a filtrate of the blood that is modified by reabsorption and secretion; urine designated for excretion moves along the ureters to the bladder.

slide6

Figure 14-2

Fluid filtered from the blood in the glomerular

capillaries is altered by reabsorption and secretion

along the length of the 1,000,000 nephrons/kidney.

slide7

Figure 14-3

Due to the hydrostatic pressure of the cardiac pump, fluid is filtered from the blood through fenestra in the glomerular capillaries into slit pores in the capsule.

slide8

Figure 14-4

The outer layer

of the kidney is

the renal cortex;

it is the site of

glomerular filtration

and the convoluted

tubules.

The inner part of

the kidney is the

renal medulla; this is

the location of the

longer loops of Henle,

and the drainage of the

collecting ducts into

the renal pelvis and ureter.

slide9

Figure 14-5

The intersection of the macula densa in the distal tubule

with the afferent and efferent arterioles forms the

juxtaglomerular apparatus, which secretes the endocrine

signal known as renin into blood in the afferent arteriole.

slide10

1. Glomerular filtration refers to the movement of fluid and solutes from the glomerular capillaries into Bowman’s space.

Figure 14-6

slide11

1. Glomerular filtration refers to the movement of fluid and solutes from the glomerular capillaries into Bowman’s space.

2. Tubular secretion refers to the secretion of solutes from the peritubular capillaries into the tubules.

Figure 14-6

slide12

1. Glomerular filtration refers to the movement of fluid and solutes from the glomerular capillaries into Bowman’s space.

2. Tubular secretion refers to the secretion of solutes from the peritubular capillaries into the tubules.

3. Tubular reabsorption refers to the movement of materials from the filtrate in the tubules into the peritubular capillaries.

Figure 14-6

slide13

Figure 14-7

Substance X is filtered and secreted but not reabsorbed.

Substance Y is filtered and some of it is reabsorbed.

Substance Z is filtered and completely reabsorbed.

slide14

Figure 14-8

Formation of the glomerular filtrate in Bowman’s capsule

is the outcome of opposing pressures:

hydrostatic pressure from the heart favors filtration, osmotic and hydrostatic pressure of the filtrate oppose it.

slide15

Figure 14-9

As vasodilation and vasoconstriction of the afferent and

efferent arterioles alter the blood flow through the

glomerular capillaries, there are corresponding alterations

in the glomerular filtration rate (GFR).

slide17

Figure 14-10

The luminal

section of the

plasma

membrane of

the tubule cells

faces the

filtrate,

whereas the

basolateral

section is in

close proximity

to the peritubular capillary.

slide18

Figure 14-11

Inulin, a biologically inert polysaccharide, can be used

to estimate the glomerular filtration rate since it is

filtered, but not reaborbed or secreted.

slide19

Figure 14-12

Release of urine from the bladder, called micturition, is coordinated by a combination of smooth and skeletal muscle relaxation and contraction.

slide21

Section B:

Regulation of Sodium, Water, and Potassium Balance:

slide24

An

consuming

ion pump in the

basolateral

membrane of the

collecting duct

cell moves Na+

toward the blood

in the peritubular

capillary . . .

ATP

Peritubular capillary

to bladder

Figure 14-13

slide25

An ATP-consuming ion pump in the

basolateral

membrane of the

collecting duct

cell moves Na+

toward the blood

in the peritubular

capillary as it produces the gradient that

facilitates Na+ entry across the luminal section of the cell . . .

Peritubular capillary

to bladder

Figure 14-13

slide26

An ATP-consuming ion pump in the

basolateral

membrane of the

collecting duct

cell moves Na+

toward the blood

in the peritubular

capillary as it produces the gradient that

facilitates Na+ entry across the luminal section of the cell; K+ movements

are in the

opposite direction.

Peritubular capillary

to bladder

Figure 14-13

slide27

Figure 14-14

When membranes are permeable to water molecules,

osmosis drives them to follow the movement of

sodium ions pumped across membranes by the ion pumps.

Water can also diffuse through adjacent tubule cells.

Sodium pumping thus accomplishes water reabsorption.

slide28

Figure 14-15

The renal counter-current multiplier system

establishes the osmotic gradient required

for the formation of hyperosmotic urine.

slide29

Figure 14-16

The geometry of the vasa recta parallels the renal counter-current multiplier system, assuring that the blood in these vessels does not “wash out” the osmotic gradient.

slide30

Figure 14-18

Alterations in GFR are mediated by a variety of neural and endocrine factors, and constitute a

major influence on the

amount of water lost

from the body in urine.

slide31

Figure 14-19

The “ACE” system is initiated by abnormally low pressure in the renal blood supply, or by other factors that cause renin secretion from the juxtaglomerular cells. Renin activates the formation of angiotensin I, which is converted to angiotensin II by Angiotensin Converting Enzyme (ACE). Angiotensin II is a vasoconstrictor (reduces GFR) and promotes the synthesis of aldosterone, an adrenal steroid hormone that increases sodium and water reabsorption in the distal tubules.

slide32

Figure 14-20

The varied pathways to

increased renin secretion

are illustrated in this chart,

as are the subsequent steps

leading to increased levels of angiotensin II in the blood.

Note that the vasoconstrictor

action of angiotensin II

allows it to decrease GFR

as a direct result of

decreasing blood flow

through the glomerular capillaries.

slide33

Figure 14-21

An abnormal increase

in blood volume “stretches out” the atria, stimulating

secretion of ANP (atrial natriuretic peptide).

ANP promotes vasodilation, thus increasing GFR, and inhibits sodium reabsorption in the distal tubule, leading to natriuresis (increased levels of sodium in urine), which increases urine volume as it decreases blood volume.

& water

slide34

Figure 14-22

An abnormal decrease

in blood volume and pressure activates baroreceptor neurons in the aorta and carotid sinuses, leading to increased secretion of vasopressin, also known as anti-diuretic hormone (ADH); which increases water permeability in the collecting ducts, which decreases the volume of excreted urine.

slide35

Figure 14-23

Drinking too much water

causes an abnormal decrease in fluid osmolarity, which alters the activity of

hypothalamic osmoreceptors,

which then reduces activity of ADH neurons, leading to decreased secretion of ADH; water permeability in the collecting ducts is reduced, thus increasing the volume of excreted urine, a condition called diuresis.

slide36

Figure 14-24

Severe loss of body water decreases GFR and increases levels

of aldosterone, vasopressin, and angiotensin II (not shown);

these adaptive responses act to promote water conservation

in the renal system to help restore blood volume and pressure.

slide37

Figure 14-25

The diversity and redundancy of signals that alter water appetite, also known as “thirst,” demonstrate the importance and adaptive value of the homeostatic maintenance of blood volume and pressure.

slide38

Figure 14-26

Potassium is filtered from the glomerular capillaries. The relative rates of potassium reabsorption and secretion are determined by the law of mass action and by aldosterone, which increases sodium reabsorption at the “expense” of increased potassium secretion.

slide39

Figure 14-27

Ingesting too much

potassium stimulates

aldosterone secretion from the adrenal cortex;

aldosterone increases

sodium reabsorption at

the “expense” of increased potassium secretion.

Also shown here is an

indication that more

potassium in the filtrate

leads to greater potassium excretion in the urine.

slide40

Figure 14-28

Decreased blood volume

and ingesting too much

potassium both stimulate

aldosterone secretion from

the adrenal cortex;

aldosterone increases

sodium reabsorption at

the “expense” of increased

potassium secretion.

slide42

Section C:

Calcium Regulation:

slide44

Figure 14-29

Osteoblasts build bone.

Osteoclasts catalyze bone degradation, when stimulated by

parathormone (PTH).

slide46

Figure 14-30

The four parathyroid glands are located adjacent to the much larger thyroid gland.

Secretion of

parathormone (PTH)

is a direct response

to an abnormal

decrease in the

concentration of

calcium ions.

slide47

Figure 14-31

Parathormone’s action to restore normal calcium levels include increased calcium reabsorption in the kidneys, increased calcium-liberating activities of osteoclasts, and increased formation of vitamin D, which increases uptake of dietary calcium in the gastrointestinal tract.

slide48

Figure 14-32

Activated 1,25 (OH)2D3 is a

steroid hormone that causes

cells in the gut to increase

the expression of genes

whose products

take up dietary calcium.

slide49

Section D:

Hydrogen Ion Regulation:

slide51

Peritubular capillary

Figure 14-33

Filtered bicarbonate

ions are “reabsorbed”

by contributing to

the generation of

new bicarbonate

ions inside the

tubule cells.

slide52

Peritubular capillary

Figure 14-34

In a person

suffering acidosis,

additional buffering

can be gained

with “new”

bicarbonate ions,

synthesized in the

tubule cells, as long

as a “sink” for

hydrogen ions (here

HPO42-) is available.

slide53

Peritubular capillary

Figure 14-35

In a person

suffering acidosis,

additional “new”

bicarbonate ions

are synthesized

from catalysis of

the amino acid

glutamine.

slide56

Section E:

Diuretics and Body Disease:

slide57

Figure 14-36

In a kidney-failure patient undergoing dialysis, the blood is briefly removed from the body to be circulated through a dialyzer, where dialysis fluid and blood move in counter current

directions to remove

nitrogenous and other wastes and adjust osmolarity before the blood

is returned to the body.