Jc. Schiltz et al., DECREASES IN ARTERIAL-PRESSURE ACTIVATE OXYTOCIN NEURONS IN CONSCIOUSRATS, American journal of physiology. Regulatory, integrative and comparative physiology, 42(4), 1997, pp. 1474-1483
Hemorrhage and nonhypotensive hypovolemia are known to increase plasma
levels of oxytocin (OT) and vasopressin (VP) in rats. The present exp
eriments demonstrated that secretion of OT and VP also are stimulated
by acute drug-induced hypotension. Injection of hydralazine abruptly d
ecreased arterial blood pressure in conscious rats and induced Fos exp
ression, a marker of neuronal activation, within OT and VP neurons in
the hypothalamus. Hydralazine also elicited substantial increases in p
lasma levels of both OT and VP. Injection of chlorisondamine similarly
elicited acute hypotension and increased plasma levels of OT and VP.
Furthermore, when the hypotensive effect of chlorisondamine was blunte
d by coinfusion of phenylephrine, the induced increases in OT and VP w
ere markedly attenuated. Across all treatments, arterial blood pressur
e was inversely related to plasma levels of OT and VP. Plasma osmolali
ty was not increased by hydralazine, nor was there evidence of gastric
malaise, two known stimuli for OT secretion in rats. These results su
ggest that arterial hypotension increases neurohypophysial release of
OT and VP in conscious rats.