Vasopressin and oxytocin secretion in chronically hyposmolar rats

Abstract

Neurohypophysial secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats maintained under hyposmolar conditions for 10-24 days. Graded intravenous infusions of hypertonic saline solutions had no consistent effect on plasma AVP and OT levels until plasma sodium concentration ([Na+]) exceeded 130 mM, after which levels of both hormones increased as an exponential function of plasma [Na+]. Detectable increases in plasma AVP and OT began at significantly lower plasma [Na+] in hyposmolar rats than in normosmolar control rats (10.8 mM lower for AVP and 18.4 mM lower for OT). AVP and OT secretion in hyposmolar rats was also markedly blunted in response to nonosmotic stimuli, including acute and chronic hypovolemia and systemic administration of cholecystokinin. Cessation of 1-desamino-8-D-arginine vasopressin-induced antidiuresis resulted in an appropriately rapid correction of plasma [Na+] to normal levels within 24 h. Consequently, although chronic hyposmolarity caused a moderate downward resetting of the osmotic thresholds for AVP and OT secretion, it did not cause sustained deficits in osmoregulation. These results suggest that osmoreceptor activity is regulated to maintain extracellular fluid and plasma osmolality within narrow absolute ranges rather than responding to relative changes in osmolality.

Galanin Inhibits Continuous and Phasic Firing in Rat Hypothalamic Magnocellular Neurosecretory Cells

“…In mammals, the secretion of vasopressin, the antidiuretic hormone, is enhanced by hyperosmolality and reduced by hypotonicity of the blood (Striker and Verbalis, 1986;Verbalis and Dohanics, 1991). Oxytocin, in turn, is well known for its role in promoting uterine contractions (Summerlee, 1981) and milk ejection (Wakerley and Lincoln, 1973).…”

“…Oxytocin, in turn, is well known for its role in promoting uterine contractions (Summerlee, 1981) and milk ejection (Wakerley and Lincoln, 1973). In the rat, however, oxytocin is also potently natriuretic , and its release is osmotically regulated in a manner analogous to that of vasopressin (Striker and Verbalis, 1986;Verbalis and Dohanics, 1991). Neurohypophysial hormone release, therefore, plays a central role in systemic osmoregulation.…”

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

“…injection of 256 pmol AM or saline vehicle, and then given access to the sucrose solution for 8 h as before. Experimental intakes were compared with sucrose intake on the day prior to experimentation Preinjection intake (ml) Postinjection intake (ml) , Verbalis & Dohanics 1991, Blackburn et al 1993. A similar experiment to the hypertonic saline studies was conducted substituting hypertonic mannitol for saline.…”

“…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.…”

Neural Activity Protects Hypothalamic Magnocellular Neurons against Axotomy-Induced Programmed Cell Death

“…Chronic hyponatremia, which inhibits secretory activity in the MCNs (Verbalis et al, 1986;Robinson et al, 1990;Verbalis and Dohanics, 1991), also produces an enhanced degeneration of the MCNs after axonal injury in the HNS (Dohanics et al, 1996). Because both of these treatments lead to decreased functional activity of the MCNs, it was suggested that there is a neuroprotective role of functional activity in the HNS after axonal injury (Herman et al, 1987;Dohanics et al, 1996).…”