Kapoor S C, Krishna G G
Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
Am J Physiol. 1991 May;260(5 Pt 2):F688-94. doi: 10.1152/ajprenal.1991.260.5.F688.
Dietary protein restriction inhibits glomerular prostaglandin (PG) synthesis and lowers plasma renin activity (PRA). To investigate the role of PG in mediating protein-induced alterations in renin secretion, male Sprague-Dawley rats were fed isocaloric diets providing either a standard 20% protein or a low-protein (6%) diet for 3 wk. An additional group of rats received a PG synthesis inhibitor, meclofenamate (25 mg/l), in the drinking water along with the 20% protein diet. Both protein restriction and meclofenamate administration significantly (P less than 0.025) lowered glomerular PGE2 production. Compared with standard protein intake, low protein intake lowered basal PRA (3.96 +/- 0.16 vs. 1.58 +/- 0.12 ng.ml-1.h-1, P less than 0.001), stimulated PRA (11.6 +/- 2.3 vs. 5.5 +/- 0.7 ng.ml-1.h-1, P less than 0.025), renal venous PRA (10.0 +/- 0.7 vs. 7.02 +/- 0.72 ng.ml-1.h-1, P less than 0.02), and plasma angiotensin II (ANG II) levels (52 +/- 5 vs. 24 +/- 3 pg/ml, P less than 0.01), while augmenting renal tissue renin content (2.36 +/- 0.21 vs. 3.56 +/- 0.30 micrograms/mg protein, P less than 0.005). Changes in plasma and renal tissue renin on meclofenamate treatment were similar to those observed on 6% protein diet. Both protein restriction and meclofenamate administration increased the glomerular ANG II receptor number, while the receptor affinity was unchanged. Thus protein restriction lowers PRA by impairing release of renin into circulation. This impairment in renin release is mediated by PG.
饮食中蛋白质限制可抑制肾小球前列腺素（PG）合成并降低血浆肾素活性（PRA）。为研究PG在介导蛋白质诱导的肾素分泌改变中的作用，将雄性Sprague-Dawley大鼠喂以等热量饮食，其中一组给予标准的20%蛋白质饮食，另一组给予低蛋白（6%）饮食，持续3周。另一组大鼠在饮用含20%蛋白质饮食的同时，给予PG合成抑制剂甲氯芬那酸（25 mg/l）。蛋白质限制和给予甲氯芬那酸均显著（P<0.025）降低了肾小球PGE2生成。与标准蛋白质摄入量相比，低蛋白质摄入量降低了基础PRA（3.96±0.16 vs. 1.58±0.12 ng·ml⁻¹·h⁻¹，P<0.001），刺激了PRA（11.6±2.3 vs. 5.5±0.7 ng·ml⁻¹·h⁻¹，P<0.025）、肾静脉PRA（10.0±0.7 vs. 7.02±0.72 ng·ml⁻¹·h⁻¹，P<0.02）以及血浆血管紧张素II（ANG II）水平（52±5 vs. 24±3 pg/ml，P<0.01），同时增加了肾组织肾素含量（2.36±0.21 vs. 3.56±0.30 μg/mg蛋白质，P<0.005）。甲氯芬那酸治疗后血浆和肾组织肾素的变化与6%蛋白质饮食时观察到的相似。蛋白质限制和给予甲氯芬那酸均增加了肾小球ANG II受体数量，而受体亲和力未改变。因此，蛋白质限制通过损害肾素释放到循环中而降低PRA。肾素释放的这种损害由PG介导。
