REGULATION OF RENAL BLOOD-FLOW BY PLASMA CHLORIDE
REGULATION OF RENAL BLOOD-FLOW BY PLASMA CHLORIDE
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DOI：
10.1172/jci110820
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发表时间：
1983-01-01
影响因子：
15.9
通讯作者：
WILCOX, CS
中科院分区：
文献类型：
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作者：
WILCOX, CS
[灰狗]的微穿刺研究表明，肾小球滤过率（GFR）随Henle袢中Na+或Cl-浓度升高而福尔斯，而离体肾脏的研究表明，GFR随渗透性利尿而福尔斯。为了确定血浆Na（PNa）、Cl（PCl）或渗透压（Posmol）急性增加的单独影响，在肾内输注高渗NaCl、NaHCO 3、醋酸钠、葡萄糖、NH 4Cl或NH 4醋酸盐至去神经支配的肾脏期间测量肾血流量（RBF）和GFR的变化。输注使实验肾脏的Posmol升高30-45 mosmol。在所有高渗输注中，RBF突然增加10-30%，表明血浆张力的急性增加导致肾血管舒张。在葡萄糖、NaHCO 3和醋酸钠输注期间，肾血管舒张持续或进一步增加，但GFR不变。相反，在输注含2Cl的溶液期间，血管舒张在1-5 min后逆转，并且RBF和GFR低于输注前水平（P < 0.01）。先前的盐耗竭使高渗NaCl输注引起的血管收缩加倍。总体而言，RBF的变化与PNa或Na分数或液体重吸收的变化无关，但与PCl（r = -0.91）和Cl-重吸收分数（r = 0.94）的变化相关。股动脉灌注2 Cl-溶液不增加股血管阻力。高钠血症引起进行性肾血管收缩和GFR下降，其独立于肾神经，通过先前的盐消耗而增强，并且与肾小管Cl-重吸收相关。氯化物诱导的血管收缩似乎对肾血管具有特异性。
Micropuncture studies [in greyhounds] have shown that glomerular filtration rate (GFR) falls in response to a rise in Na+ or Cl- concentrations in the loop of Henle, whereas studies in isolated kidneys have shown that GFR falls in response to osmotic diuresis. To define the separate effects of an acute increase in plasma Na (PNa), Cl (PCl) or osmolality (Posmol), changes in renal blood flow (RBF) and GFR were measured during intrarenal infusions of hypertonic NaCl, NaHCO3, Na acetate, dextrose, NH4Cl or NH4acetate to denervated kidneys. The infusions raised Posmol at the experimental kidney by 30-45 mosmol. RBF increased abruptly by 10-30% with all hypertonic infusions indicating that an acute increase in plasma tonicity causes renal vasodilatation. Renal vasodilatation persisted or increased further during infusion of dextrose, NaHCO3 and Na acetate, but GFR was unchanged. In contrast, during infusion of the 2 Cl-containing solutions, vasodilatation was reversed after 1-5 min and RBF and GFR decreased (P < 0.01) below preinfusion levels. Prior salt depletion doubled the vasoconstriction seen with hypertonic NaCl infusions. Overall, changes in RBF were unrelated to changes in PNa or fractional Na or fluid reabsorption but correlated with changes in PCl (r = -0.91) and fractional Cl- reabsorption (r = 0.94). The intrafemoral arterial infusion of the 2 Cl-containing solutions did not increase femoral vascular resistance. Hyperchloremia produces a progressive renal vasoconstriction and fall in GFR that is independent of the renal nerves, is potentiated by prior salt depletion and is related to tubular Cl- reabsorption. Chloride-induced vasoconstriction appears specific for the renal vessels.