Abboud H E, Luke R G, Galla J H, Kotchen T A
Circ Res. 1979 Jun;44(6):815-21. doi: 10.1161/01.res.44.6.815.
To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 M NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131I]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0 +/- 1.0 ng/ml per hr, mean +/- SEM) was increased (P less than 0.05) over PRA1 (4.7 +/- 0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1 = 5.3 +/- 0.7, PRA2 = 6.1 +/- 0.7, P = NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 weeks on a low salt diet. PRA2 (47 +/- 5 ng/ml per hr) was increased as compared to PRA1 (24 +/- 2 ng/ml per hr, P less than 0.005) in the Cl-depleted group but not in the control group (PRA1 = 24 +/- 3, PRA2 = 27 +/- 6 ng/ml per hr, P = NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41 +/- 6 ng/ml per hr) was significantly elevated as compared to PRA1 (25 +/- 4 ng/ml per hr, P less than 0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36 +/- 6 ng/ml per hr, P less than 0.05) as compared to PRA1 (23 +/- 4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.
为了确定单纯急性氯化物缺乏是否会刺激肾素分泌，我们通过腹膜透析（PD），用0.15M碳酸氢钠或0.15M硝酸钠对大鼠进行无钠缺乏的选择性氯化物缺乏处理。对照大鼠用0.15M氯化钠进行透析。在腹膜透析前（PRA1）和腹膜透析105分钟后（PRA2）测量血浆肾素活性（PRA）。腹膜透析后通过输注无盐白蛋白使血浆容量扩张，并在PRA2测量后立即用[131I]白蛋白进行测量。在实验1中，大鼠采用正常饮食。氯化物缺乏组的PRA2（每小时7.0±1.0ng/ml，平均值±标准误）较PRA1（每小时4.7±0.7ng/ml）升高（P<0.05），而对照组未升高（PRA1 = 5.3±0.7，PRA2 = 6.1±0.7，P = 无显著性差异）。在实验2中，为了造成更大程度的氯化物缺乏，所有大鼠采用低盐饮食准备2周。氯化物缺乏组的PRA2（每小时47±5ng/ml）较PRA1（每小时24±2ng/ml，P<0.005）升高，而对照组未升高（PRA1 = 24±3，PRA2 = 27±6ng/ml，P = 无显著性差异）。这些氯化物缺乏的大鼠血清钾和最终血浆容量略低于对照组，但无显著性差异。为了排除这两种刺激对肾素的叠加效应，在实验2a中，我们给氯化物缺乏的大鼠输注的白蛋白量是对照组的三倍，并加入100mEq/升的碳酸氢钾。尽管容量扩张和钾负荷增加，PRA2（每小时41±6ng/ml）较PRA1（每小时25±4ng/ml，P<0.01）仍显著升高。由于所有氯化物缺乏且肾素受刺激的大鼠均存在急性代谢性碱中毒，另外一组（2b）用0.
