Mechanisms of centrally administered et 1-induced increases in systemic arterial pressure and avp secretion. Rossi, Noreen F., and Haiping Chen. Departments of Medicine and Physiology, Wayne State University School of Medicine and Department of Veterans Affairs Medical Center
APStracts 3:0196E, 1996.
Endothelins (ETs) within the CNS alter systemic cardiovascular responses and vaso pressin (AVP) secretion. These experiments were designed to ascertain whether the rise in systemic arterial pressure after central administration of ET 1 is mediated by enhancing sympa thetic outflow and/or circulating AVP. In Long Evans (LE/LE) rats, intracerebroventricular injection of 1 to 10 pmol ET 1 dose dependently increased mean arterial pressure (MAP). Peak response occurred 7 to 12 minutes after ET 1 and was inhibited by ETA receptor antago nism. Systemic V1 receptor blockade did not inhibit the pressor response, and rats with central diabetes insipidus (DI/DI) displayed an identical rise in MAP. Ganglionic blockade prevented ET 1-induced hemodynamic effects. Peak plasma AVP levels occurred 60 minutes after ET 1, as the pressor response began to wane. In sinoaortic denervated LE/LE rats, ET 1 elicited a 10-fold increase in AVP secretion that coincided with the hemodynamic changes and was blocked by BQ 123. Thus, ET 1 via ETA receptors within the CNS induced a concentration dependent increase in systemic arterial pressure mediated by enhanced sympathetic outflow but not by circulating AVP. Reflex baroreceptor activation attenuated AVP release. 

Received 1 July 1996; accepted in final form 12 September 1996.
APS Manuscript Number E309-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996