Clinical Correlates for insulin

1. Clinical correlates (posterior
pituitary)
Dr. H. O. Jimoh-Abdulghaffaar
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2. Outline
• Introduction
• Hormones
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3. Introduction
• Otherwise known as neurohypophysis.
• Not actually a gland but, rather, an extension of the neural
components of the hypothalamus.
• The axons of two well-defined clusters of hypothalamic neurons (the
supraoptic and paraventricular nuclei) pass down the infundibulum
and end within the posterior pituitary in close proximity to capillaries.
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4. Posterior pituitary hormones
• Synthesized in the cell bodies of the supra-optic and paraventricular
nuclei of the hypothalamus.
• The axons of the neurons pass down the infundibulum to terminate in
the posterior pituitary.
1. oxytocin
2. vasopressin (anti-diuretic hormone ADH)
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5. Fig. 1: Hypothalamo-hypophyseal tract
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6. Oxytocin
• Actions:
A. Humans
1. Breast: contraction of smooth muscles cells, milk ejection during lactation.
2. Uterus: contraction of smooth muscles cells, fetal expulsion during
parturition.
B. Other mammals
1. Memory
2. Behaviuor e. g. pair bonding, maternal behavior, and emotions such as love.
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7. Clinical correlates of oxytocin
1. Postpartum depression: Oxytocin level is said to be low in women
with this condition.
2. Oxytocin is put in the IV fluid of women who just gave birth to aid
expulsion of placenta
3. Uterine artery and blood vessels doesn't constrict after parturition
in women without oxytocin leading to severe bleeding.
4. There can be oxytocin receptor failure in the uterus
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8. Vasopressin
• Action:
1. Blood vessels: contraction of smooth musccle cells, vasoconstriction,
increased blood pressure.
2. Kidneys: decrease water excretion
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9. • Vasopressin facilitate binding of AQ to cell
• Aids water reabsorption in collecting duct from lumen into the cell.
• Deficiency of vasopressin in patients prevents binding of AQ2 hence
water isn't being reabsorbed, more water is then secreted into urine,
leaving them dehydrated.This is termed water diuresis
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10. Clinical correlates of vasopressin
1. Water diuresis
• Vasopressin from the blood enters the interstitial fluid and binds to its receptor on the basolateral
membrane, leading to increased intracellular production of the second-messenger cAMP.
• cAMP activates the enzyme cAMP-dependent protein kinase (also called protein kinase A or PKA),
which, in turn, phosphorylates proteins that increase the rate of fusion of vesicles containing AQP2 with
the apical membrane.
• This leads to an increase in the number of AQP2s inserted into the apical membrane from vesicles in
the cytosol.
• This allows an increase in the diffusion of water down its concentration gradient across the apical
membrane into the cell.
• Water then diffuses through AQP3 and AQP4 water channels on the basolateral membrane into the
interstitial fluid and enters the blood.
• There is increased permeability of the collectimg duct and water reabsorption is maximal with < 1%
being filtered.
• low vasopressin causes decreased water reabsorption and large volume of water is exccreted in urine -
water diuresis.
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11. Clinical correlates of vasopressin
2. Diabetes insipidus
Permeability of the collecting duct to water is low.
a. Central
failure of the axons with cell bodies in the hypothalamus
and synapses on blood vessels in the posterior pituitary to
synthesize or release vasopressin.
b. Nephrogenic
inability of the kidneys to respond to vasopressin.Receptors
are either downregulated or absent
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• Thiazide diuretics act on collecting duct using d principle of water
reabsorption in collecting duct, hence blood vol will be increased and
blood pressure will fall(management of hypertension)