Abstract

In urethane-anesthetized rats, injections of 50 pmol of arginine-vasopressin (AVP) or thyrotropin-releasing hormone (TRH) into a lateral cerebral ventricle (i.c.v.) elicit short-latency increases in blood pressure, i.c.v. injection of 50 pmol of the AVP antagonist, d(CH 2) 5Tyr(Me)AVP, but not of the vehicle (artificial cerebrospinal fluid; aCSF), abolished the pressor action of i.c.v. AVP. The AVP antagonist did not antagonize the TRH-induced pressor responses. In another group of rats, a monopolar stainless-steel electrode was positioned stereotaxically in the paraventricular nucleus (PVN) and pressor responses were elicited by electrical stimulation of the PVN. Micro-injection of 1 nmol of the AVP antagonist, but not of aCSF alone, into the nucleus tractus solitarius/vagal area (NTS/VA), reduced PVN-stimulated pressor responses to 26 ± 6% of control and stimulation-induced tachycardia to 37.3 ± 9.0% of control. These studies indicate that the pressor and heart-rate responses to PVN stimulation may be mediated, in part, via AVP receptors in the NTS/VA.

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