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(Hypertension. 2003;41:583.)
© 2003 American Heart Association, Inc.

Scientific Contributions

Role of Angiotensin II in the Neural Control of Renal Function

Marie E. Le Fevre; Sarah-Jane Guild; Rohit Ramchandra; Carolyn J. Barrett; Simon C. Malpas

From the Circulatory Control Laboratory, Department of Physiology, University of Auckland, Auckland, New Zealand.

Correspondence to Dr Simon C. Malpas, Circulatory Control Laboratory, Department of Physiology, University of Auckland Medical School, Private Bag 92019, Auckland, New Zealand. E-mail s.malpas{at}auckland.ac.nz

The aim of the present study was to distinguish between the direct effects of the renal nerves on renal function and indirect effects via neurally mediated increased systemic angiotensin II. We applied low-level electrical stimulation (1 Hz) to the left renal nerves in pentobarbitone-anesthetized rabbits for 180 minutes and measured renal blood flow, sodium excretion, and urine flow rate from both the stimulated and the nonstimulated contralateral kidney in the presence and the absence of ACE inhibition (enalaprilat). Stimulation resulted in an angiotensin II–mediated rise in arterial pressure and decreases in renal blood flow, urine flow rate, and sodium excretion on the stimulated side. On the nonstimulated denervated side, we found no change in renal blood flow, but found a decrease in urine flow rate. With ACE inhibition, renal stimulation no longer caused an increase in arterial pressure, the antidiuretic responses of the stimulated kidney were attenuated, and, importantly, the decrease in urine flow rate on the nonstimulated kidney was completely abolished. We therefore propose that although a direct effect of the renal nerves on sodium excretion is clearly present, the antidiuresis and antinatriuresis observed during renal activation is further supported by a neurally mediated increase in systemic angiotensin II.

Key Words: sympathetic nerve activity • renal blood flow • rabbit • antidiuresis • antinatriuresis

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