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AJP - Endocrinology and Metabolism, Vol 266, Issue 2 E230-E241, Copyright © 1994 by American Physiological Society
ARTICLES |
A. Nakamura and E. J. Johns
Department of Physiology, Medical School, Birmingham, West Midlands, United Kingdom.
In this study, we try to determine the influence of renal nerve activity on renal function, plasma renin activity (PRA), and the corresponding expression of renin and angiotensinogen genes in the kidney. In pentobarbitone-anesthetized rats, the left renal nerves were stimulated (15 V, 0.2 ms) at frequencies to reduce left renal blood flow by 15, 30, and 45%. There were corresponding reductions in glomerular filtration rate from 12 to 52% and absolute and fractional sodium excretions from 20 to 75%. PRA levels in control rats were 10.8 +/- 1.5 and were increased to 65.9 +/- 9.1, 144.2 +/- 19.7, and 277.2 +/- 22.0 ng angiotensin I.h-1.ml-1 after 1 h at each of the three levels of nerve stimulation. Renal renin mRNA was similar in innervated and denervated kidneys and was not affected by the lowest level of nerve stimulation; however, neurally induced decreases in blood flow to 30 and 45% increased renin mRNA levels by 3.0- and 3.4-fold (both P < 0.05), respectively. Angiotensinogen mRNA levels were higher (P < 0.05) in kidneys subjected to the lowest level of nerve stimulation, but when renal blood flow was reduced by 30 and 45%, expression of this gene was unchanged. Stimulation of the renal nerves in the presence of the beta 1-adrenoceptor antagonist atenolol only doubled PRA at the highest rates of stimulation. Neither renal renin nor angiotensinogen mRNA were changed during neurally mediated reductions in renal blood flow of 15 or 30% after administration of atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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