Release of oxytocin induced by salt loading and its influence on renal excretion in the male rat.

Abstract

SUMMARY1. The present study investigates the nature and magnitude of the renal response to plasma levels of oxytocin which might be induced by salt loading.2. Increased plasma osmolality induced by loading with NaCl is an effective stimulus for oxytocin release in the unanaesthetized male rat. Plasma oxytocin concentration was positively correlated (r = 0.77) with plasma osmolality. Plasma oxytocin (,uu./ml.) = 0 37 x (plasma osmolality (m-osmole/kg) -297).3. In anaesthetized Long Evans rats intra-atrial administration of oxytocin at rates of 0*05 and 0.15 m-u./ml. produced plasma hormone concentrations (5 + 1 and 16 + 2 ,uu./ml. respectively) within the range induced by salt loading. 6. Plasma ocytocin levels similar to those induced by severe dehydration or salt loading are effective in increasing renal Na+ and Cl-excretion and urine flow. These effects on water and electrolyte excretion appear to be independent of each other and both may be modified by the presence or absence of vasopressin.7. This study provides no evidence for a major role for oxytocin in the day to day regulation of salt or water balance under conditions of normal hydration in the male rat.

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

“…The different potencies of these hormones can be attributed to a relative affinity of OT for its own receptor or its lower affinity for V2 and V1 AVP receptors. On the other hand, studies have suggested a synergistic Neurohypophyseal hormones, ANP and nitrergic system effect of AVP and OT actions on the inner medullary collecting duct where both peptides induce an increase in cAMP accumulation and natriuresis (24,29). OT binds to the V2 AVP receptor because of its structural similarity to AVP.…”

“…It has long been recognized that OT increases renal electrolyte excretion in various species, and that the natriuretic and kaliuretic effects are AVP independent. OT and AVP are secreted simultaneously in response to hyperosmolality and hypovolemia (19,24,25) and when systemically administered (iv or ip) induce natriuresis (26,27). OT is a more potent natriuretic hormone than AVP.…”

A possible relationship between brain-derived adrenomedullin and oxytocin in the regulation of sodium balance

“…Salt loading an animal will lead to significant increases in tissue Ot mRNA levels and plasma OT concentrations (Balment et al 1980, Van Tol et al 1987, Dellmann et al 1988, Verbalis & Dohinics 1991, Ozaki et al 2004. The effects of altered central AM levels on hypertonic saline-stimulated plasma OT levels were evaluated.…”

“…Both the PVN and SON contain neurons that produce arginine vasopressin (AVP) and/or oxytocin (OT) and project not only to the posterior pituitary gland, but also elsewhere within the central nervous system (CNS). While AVP is well known to control fluid balance by its antidiuretic action, OT, particularly when acting as a neurotransmitter, has been implicated as an important regulator of sodium balance (Balment et al 1980, Van Tol et al 1987, Blackburn et al 1992a,b, 1993, Verbalis et al 1995, Amico et al 2001, Fitts et al 2003, Rigatto et al 2003. We have previously demonstrated that brain-derived AM is a physiologic regulator of AVP secretion (Taylor et al 2005).…”

“…Indeed, i.v. infusion of hypertonic saline or chronic salt loading in rats led to increased plasma OT levels (Balment et al 1980, Vant Tol et al 1987, Verbalis & Dohanics 1991, Verbalis et al 1995. Not only does sodium stimulate OT production and release, but also OT acting within CNS sites inhibits further NaCl consumption, providing a negative feedback loop to maintain sodium homeostasis.…”