Hemodynamic and microvascular responses in the hindquarters during the development of renal hypertension in rats. Evidence for the involvement of an autoregulatory component.

Abstract

Microvascular responses in the cremaster muscle were compared with changes in mean arterial pressure and hindquarters vascular resistance during the development (initial 3 hours) of two-kidney one-clip renal hypertension in rats, to examine the possibility that an autoregulatory mechanism may contribute to the development of hypertension. Rats were anesthetized with urethane and chloralose and implanted with Doppler flow probes on the renal artery and abdominal aorta. Acute hypertension was produced by inflation of a balloon occluder on the renal artery to reduce renal flow by 50%. The cremaster muscle was isolated with intact innervation and circulation for measurement of microvessel diameters. To determine whether increased pressure contributed to the changes in hindquarters vascular resistance or in microvascular diameters during acute hypertension, arterial pressure was prevented from increasing in the hindquarters region after renal artery stenosis by servo-controlled inflation of a balloon occluder around the sacral aorta to maintain hindquarters pressure at normotensive levels. In hypertensive rats with unprotected hindquarters, mean arterial pressure and hindquarters vascular resistance increased 26% and 20%, respectively, after renal artery stenosis. In comparison, hypertensive rats with protected hindquarters exhibited a similar increase in mean arterial pressure, but hindquarters vascular resistance was significantly reduced compared to that in hypertensive rats with unprotected hindquarters. In the cremaster microcirculation, vasoconstriction was observed only in the small third- (mean +/- SEM: 29 +/- 4 micron) and fourth- (12 +/- 2 micron) order arterioles in rats with unprotected hindquarters. In general, microvessel diameters in rats with protected hindquarters that had lower hindquarters vascular resistance than those with unprotected hindquarters were larger for the second- (82 +/- 5 micron), third-, and fourth-order arterioles, suggesting less vasoconstrictor tone. Our data indicate that the increase in hindquarters resistance during the development of renal hypertension is, in part, dependent on the presence of a pressure-dependent autoregulatory process.