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. 1987 Nov;253(5 Pt 2):F1051-7.
doi: 10.1152/ajprenal.1987.253.5.F1051.

Control of renin release by dietary NaCl in the rat

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Control of renin release by dietary NaCl in the rat

W J Welch et al. Am J Physiol. 1987 Nov.

Abstract

The purpose of the present study is to determine whether changes of plasma renin activity (PRA) induced by dietary NaCl are mediated by a renal tubular mechanism or by a neural mechanism. Male Sprague-Dawley rats were placed on low-, normal-, or high-NaCl diets for 1 wk (n = 8 for each group). There were no group differences of glomerular filtration rate (GFR), renal plasma flow, Na+ or Cl- delivery to the loop, Na+ or Cl- reabsorption in the loop, Na+ or Cl- concentration in early distal tubular fluid, or Na+ or Cl- delivery to the early distal tubule. PRA of rats on normal NaCl (4.8 ng.ml-1.h-1 +/- 0.8) was greater (P less than 0.05) than that of rats on high NaCl (3.3 +/- 0.4) and less (P less than 0.05) than that of animals on low NaCl (9.1 +/- 1.8). To determine whether alterations of PRA by dietary NaCl might be related to low-pressure baroreceptors with vagal afferents, animals were bilaterally vagotomized after micropuncture. Forty-five minutes after vagotomy, PRA increased (P less than 0.05) on each of the diets, however, after vagotomy mean PRA in animals fed normal (10.9 +/- 1.8) and low NaCl (13.2 +/- 2.2) did not differ. Thus our results do not support the hypothesis that suppression of PRA by dietary NaCl loading is related to a renal tubular mechanism. A vagally mediated mechanism may contribute to renin suppression by dietary NaCl.

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