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大鼠饮食中氯化钠对肾素释放的控制。

Control of renin release by dietary NaCl in the rat.

作者信息

Welch W J, Ott C E, Lorenz J N, Kotchen T A

机构信息

Department of Medicine, University of Kentucky School of Medicine, Lexington 40536.

出版信息

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

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.

摘要

本研究的目的是确定饮食中氯化钠引起的血浆肾素活性(PRA)变化是由肾小管机制还是神经机制介导的。将雄性Sprague-Dawley大鼠置于低、正常或高氯化钠饮食中1周(每组n = 8)。各组在肾小球滤过率(GFR)、肾血浆流量、到达髓袢的Na⁺或Cl⁻量、髓袢中的Na⁺或Cl⁻重吸收、远端小管起始段液体中的Na⁺或Cl⁻浓度或到达远端小管起始段的Na⁺或Cl⁻量方面没有差异。正常氯化钠饮食组大鼠的PRA(4.8 ng·ml⁻¹·h⁻¹±0.8)高于高氯化钠饮食组大鼠(3.3±0.4,P<0.05),低于低氯化钠饮食组动物(9.1±1.8,P<0.05)。为了确定饮食中氯化钠引起的PRA改变是否可能与具有迷走传入神经的低压压力感受器有关,在微穿刺后对动物进行双侧迷走神经切断术。迷走神经切断术后45分钟,每种饮食的PRA均升高(P<0.05),然而,迷走神经切断术后,正常饮食(10.9±1.8)和低氯化钠饮食(13.2±2.2)的动物平均PRA没有差异。因此,我们的结果不支持饮食中氯化钠负荷抑制PRA与肾小管机制有关的假设。迷走神经介导的机制可能有助于饮食中氯化钠对肾素的抑制作用。

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