Neural contribution to renal hypertension following acute renal artery stenosis in conscious rats.

Abstract

To assess the hemodynamic changes during acute renal artery stenosis (RSt) and their dependence on alterations in the renin-angiotensin and sympathetic nervous systems, we studied conscious rats chronically instrumented with miniaturized pulsed-Doppler flow probes. Probes were implanted on the superior mesenteric and both renal arteries, and on the lower abdominal aorta for measurement of mesenteric (MR), renal (RR), and hindquarters (HQR) vascular resistance. Unilateral RSt, with a pneumatic cuff occluder that reduced flow by approximately 50%, increased mean arterial pressure (MAP) by 32%, reduced heart rate, and increased MR, nonstenotic (contralateral) RR and HQR. The hypertension was renin-dependent since plasma renin activity increased 6-fold and the angiotensin II (AII) antagonist, saralasin, significantly reduced MAP and regional resistances. The acute hypertension was also associated with increased neurogenic vasoconstrictor tone since hexamethonium markedly reduced MAP, MR, HQR and non-stenotic RR. Hexamethonium similarly decreased MAP during hypertension induced by AII infusion, whereas hypertension produced by the "pure" peripheral vasoconstrictor, phenylephrine, was unaffected by ganglionic blockade. In animals with peripheral sympathectomy produced by 6-hydroxydopamine, acute RSt produced hemodynamic changes similar in magnitude to intact animals; however, PRA increased 3-fold more than in intact rats. We conclude that hypertension induced by acute RSt in conscious rats is not only renin-dependent, but is also associated with inappropriately high neurogenic vasoconstrictor tone, presumably activated by indirect neural actions of AII.