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AJP - Renal Physiology, Vol 264, Issue 3 515-F522, Copyright © 1993 by American Physiological Society
ARTICLES |
W. A. Cupples
Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.
Release of a suprarenal aortic clamp results in angiotensin-dependent, arterial pressure-mediated renal vasoconstriction. The experiments reported here were designed to show whether this represents operation of autoregulation and whether the slow component of autoregulation is affected by angiotensin II (ANG II). They were performed using halothane-anesthetized Sprague-Dawley rats. In the 1st experiment renal perfusion pressure (RPP) was reduced in steps from spontaneous level to 45 mmHg and then returned in steps to the spontaneous level. The autoregulatory plateau was left-shifted some 20-30 mmHg, with the lower limit of autoregulation reduced from approximately 85 mmHg on the downward leg to approximately 60 mmHg on the upward leg. This resetting was blocked by captopril. Two experiments examined low pressure autoregulation in more detail. After RPP was reduced, three pairs of steps between 65 and 75 mmHg were performed. Significant renal vasodilatation was observed after downward pressure steps in both experiments. Time constants (tau) of resistance adjustment were recovered from most steps by curve fitting. In both experiments tau down = 0.07 +/- 0.01 Hz was faster than tau up = 0.04 +/- 0.01 Hz. Blockade of ANG II by enalaprilat or by the AT1-receptor blocker losartan potassium significantly inhibited regulatory vasodilatation and vasoconstriction at low RPP. Also, tau down = 0.04 +/- 0.01 Hz collapsed to the value of tau up = 0.04 +/- 0.01 Hz. These results demonstrate a significant role for ANG II in renal autoregulation. They show that ANG II is necessary for autoregulation to reset to operate at reduced arterial pressure and to defend a lower blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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