Abstract
Vasopressin (VP) and oxytocin (OT) are mainly synthesized in the magnocellular neurons of the paraventricular (PVN) and supraoptic nucleus (SON) of the hypothalamus. Axons from the magnocellular part of the PVN and SON project to neurohypophysis where VP and OT are released in blood to act like hormones. Axons from the parvocellular part of PVN project to extra-hypothalamic brain areas (median eminence, limbic system, brainstem and spinal cord) where VP and OT act like neurotransmitters/modulators. VP and OT act in complementary manner in cardiovascular control, both as hormones and neurotransmitters. While VP conserves water and increases circulating blood volume, OT eliminates sodium. Hyperactivity of VP neurons and quiescence of OT neurons in PVN underlie osmotic adjustment to pregnancy. In most vascular beds VP is a potent vasoconstrictor, more potent than OT, except in the umbilical artery at term. The vasoconstriction by VP and OT is mediated via V1aR. In some vascular beds, i.e. the lungs and the brain, VP and OT produce NO dependent vasodilatation. Peripherally, VP has been found to enhance the sensitivity of the baro-receptor while centrally, VP and OT increase sympathetic outflow, suppresse baro-receptor reflex and enhance respiration. Whilst VP is an important mediator of stress that triggers ACTH release, OT exhibits anti-stress properties. Moreover, VP has been found to contribute considerably to progression of hypertension and heart failure while OT has been found to decrease blood pressure and promote cardiac healing.
Highlights
Neurohypophyseal peptides vasopressin (VP) and oxytocin (OT) are mainly synthesized in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) of the hypothalamus
In freely moving conscious rats exposed to graded hemorrhaged, using the same selective antagonists, we found that VP modulates blood pressure (BP) short-term variability both under nonhypotensive and hypotensive conditions, and that only V2R blockade potentiated hemorrhage-induced bradycardia and prevented the increase of low-frequency BP short-term variability [58] linked to renal sympathetic nerve activity (RSNA) [93]
Using the advantages of spectral analysis technique that provide a dynamic insight into cardiorespiratory control [114], Milutinovi and coworkers [59] have shown that, endogenous increase of VP concentration in the brain during exposure of rats to stress by immobilization, enhances the respiration induced high-frequency blood pressure variability and sympathetically-mediate LF-BP variability directed to blood vessels [139, 140]
Summary
Neurohypophyseal peptides vasopressin (VP) and oxytocin (OT) are mainly synthesized in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) of the hypothalamus. These studies revealed that loading stretch receptors at veno-atrial junction engender a unique differential pattern of sympathetic activity to the heart and the kidney via PVN direct projections to the intermediolateral column of the spinal cord: OTR receptors were found to mediate cardiac sympathetic activation and tachycardia while V1aR receptors were found to produce renal symaptho-inhibition, with consequent renal vasodilatation and diuresis.
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