The following points highlight the two categories of non-peptide hormones produced by posterior pituitary. The categories are: 1. Functions of Vasopressin 2. Functions of Oxytocin.
Category # 1. Functions of Vasopressin:
(1) Antidiuretic effect:
In mammals, following a rise in plasma osmolarity, vasopressin or antidiuretic hormone (ADH) binds to V2 receptors on the basolateral plasma membrane of the distal tubules and collecting ducts of renal nephrons. This triggers the signal transduction through adenylate cyclase-cAMP system in these cells and finally leads to an increase in membrane permeability to water.
This enhances the osmotic reabsorption of water from the tubular lumen to the surrounding hypertonic medullary interstitium. The hormone consequently produces hypertonic urine having low volume, low flow rate, high specific gravity and high concentration of Na+, Cl−, H2PO4− and urea.
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ADH also increases the permeability of medullary collecting ducts to urea. Thus, it enhances the reabsorption of urea by diffusion from the tubular filtrate. This urea contributes to the hyper-tonicity of medullary interstitium and consequently to the antidiuretic effects of vasopressin.
(2) Pressor effect:
In response to a critical fall in either the volume or the pressure of blood, vasopressin binds to the V1 receptors on the vascular smooth muscle walls. This raises Ca2+ and Ca2+-calmodulin in smooth muscles which then bind to and activates the myosin light chain kinase leading to actin- myosin interaction. As a result, the arteriolar smooth muscles contract and raise the peripheral resistance and arterial blood pressure.
Category # 2. Functions of Oxytocin:
(1) Lactation:
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Stimulation of the nipple produces a neuro-endocrinal reflex that causes secretion of oxytocin. In turn, the hormone increases cytoplasmic Ca2+ concentration in the myoepithelial cells around mammary alveoli and ducts and in the smooth muscle cells around mammary milk sinuses. It thereby brings about their contraction with a consequent ejection of the stored milk.
(2) Parturition:
At the full-term of pregnancy as the foetus enters the birth canal, the lower segment of the uterus, the cervix and then the vagina are dilated and this causes reflex release of oxytocin. Oxytocin causes contraction of uterine muscles for child birth. Strong uterine contractions cause further descent of the fetus, further distention and further release of oxytocin.
(3) Oxytocin is an effective natriuretic agent particularly at low rates of urine flow and so it may be involved in the regulation of sodium balance.
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Regulation of vasopressin and oxytocin secretion:
Neuro-hypophyseal secretion of vasopressin and oxytocin is not under the control of hypothalamic hormones, but their secretions are regulated by neuronal controls.
Vasopressin:
(a) Stimulation of hypothalamic osmoreceptors following a rise in plasma osmoconcentration causes vasopressin release from posterior pituitary. In contrast, a fall in plasma osmolality decreases vasopressin release. A little rise in plasma osmolality causes steep and linear rise in vasopressin release.
(b) Nerve impulses generated by (i) stimulation of carotid and aortic baroreceptors by hypotension resulting from a severe fall in blood volume or (ii) stimulation of left arterial volume receptors following a fall in blood volume (e.g. in case of haemorrhage), may cause immediate release of vasopressin.
Oxytocin:
(a) Conditioned and unconditioned suckling reflexes generated by nerve impulses from nipple receptors during suckling cause release of oxytocin.
(b) Dilatation of uterine cervix by the full-term foetus at the time of parturition stimulates the uterine stretch receptors that in turn cause oxytocin release.