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oxytocin and vasopressin n.
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Oxytocin and Vasopressin

Oxytocin and Vasopressin

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Oxytocin and Vasopressin

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  1. Oxytocin and Vasopressin Posterior Hypothalamus – Posterior Pituitary • Oxytocin • Vasopressin (ADH)

  2. PVN SON Hypothalamo-Hypophyseal Axis PVN: Paraventricular nucleus SON: Supraoptic nucleus

  3. Hypothalamus – Posterior Pituitary

  4. Neurosecretion

  5. Chemical Structures of Oxytocin and Vasopressin

  6. Oxytocin and ADH in blood circulation • Carried without binding to plasma proteins • Very short half-lives (5-10 min)

  7. Oxytocin and Vasopressin

  8. Feed-Back Control of Oxytocin Secretion

  9. Role of oxytocin in parturition Effect on myometrium: contraction

  10. Other Effects of Oxytocin • Plays a role in development of motherhood behavior or instinct • Can act as a neurotransmitter in the CNS • Involved in learning and memory

  11. Effects of ADH on distal tubules and collecting ducts in the nephron and water reabsorption ADH

  12. Increased plasma osmolarity increases ADH secretion • Role of osmoreceptors in the hypothalamus

  13. Effect of ADHon Vascular Smooth Muscle • Produces strong vasoconstrictive effects • This vasoconstriction is especially important in cases of severe hypovolemia and hypotension

  14. ADH Receptors • V1receptors are found in the vascular smooth muscle and responsible for the effects there • V2receptors are found incollecting tubules and responsible for the effects in the kidneys • cAMP second messenger system – ADH • Aquaporin-2 molecules(water channel protein)in collecting duct cells and ADH

  15. Stimulation of baroreceptors in the aort as a result of hypotension stimulates ADH secretion • Deficiency of venous return to atriums increases ADH secretion or vice versa

  16. DIABETES INSIPIDUSClinical picture of ADH deficiency • Etiology: • Trauma • Tumor • Idiopatic • Genetic • Other lesions affecting the hypothalamus or posteriorpituitary • Or nephrotic diabetesinsipidus

  17. DIABETES INSIPIDUS Pathophysiology • In ADH deficiency, patients cannot consantrate urine. Therefore, water deficit and hyperosmolarity develop • As water deficit continues, thirst and related signals increase • Poliuria and polydypsiaare characteristic • If sufficient water is not taken, hypernatremia develops

  18. SYNDROME OF INAPPROPRIATE ADH (SIADH) • Menengitis • CNS diseases • Head traumas • Pulmonary diseases • Cirrhosis Syndrome of excessive secretion of ADH

  19. Urine dilution is reduced • Total extracellular fluid increases, there is hypotonicity • Mild cases may present asymptomatic (Na>120) • Na <110, lethargy, convulsions, coma and death can develop SYNDROME OF INAPPROPRIATE ADH (SIADH) • Treatment: • Removal of the cause • Water intake is reduced • Demeclocycline suppresses ADH receptors in the distal tubules and collecting ducts and thus causes nephrogenic DI