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Am J Physiol Endocrinol Metab 279: E18-E24, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 1, E18-E24, July 2000

Endothelin-1 in hypertension in the baroreflex-intact SHR: a role independent from vasopressin release

Noreen F. Rossi1,2, Donal S. O'Leary2, Dixon Woodbury2, and Haiping Chen1

Departments of 1 Medicine and 2 Physiology, Wayne State University School of Medicine, and John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan 48201

This study sought to identify whether central endothelin (ET) receptor activation contributes to the elevated pressure in spontaneously hypertensive rats (SHR) and whether an ET-stimulated vasopressin (AVP) release mediates the increased pressure. In Wistar Kyoto (WKY) rats, intracerebroventricular ET-1 induced a dose-dependent pressor response that was shifted rightward in SHR. ETA antagonism decreased mean arterial pressure in baroreflex-intact SHR (P < 0.01), consistent with inhibition of endogenous ET-1, and blocked the pressor response to exogenous ET-1 in both strains. ET-1 increased AVP only after sinoaortic denervation (P < 0.05). Contrary to WKY, sinoaortic denervation was required to elicit a significant pressor response with 5 pmol ET-1 in SHR. Sinoaortic denervation permitted ET-1 to increase AVP in both strains, and peripheral V1 blockade decreased pressure in denervated but not intact rats. After nitroprusside normalized pressure in SHR, the pressor and AVP secretory responses paralleled those in WKY. Thus endogenous ETA receptor mechanisms contribute to hypertension, independent of AVP, in baroreflex-intact SHR. Although blunted in the hypertensive state, the arterial baroreflex buffers the ET-1-induced pressor and AVP secretory responses in both strains.

antidiuretic hormone; arterial baroreflex; blood pressure; spontaneously hypertensive rat; Wistar Kyoto rat


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