Effects of a calcium channel agonist on renin release from perfused rat kidneys.

Renal physiology Pub Date : 1986-01-01 DOI:10.1159/000173092
J R Dietz
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引用次数: 6

Abstract

The effects of a calcium channel agonist, BAY K-8644, on renin release and renal function were examined in perfused rat kidneys. BAY K-8644 increased renal vascular resistance and reduced glomerular filtration rate, sodium excretion and urine flow in a dose-dependent manner. These actions were prevented by the calcium channel blocker nifedipine. BAY K-8644 had no significant effect on basal renin secretion and failed to prevent renin stimulation by low-perfusion pressure or isoproterenol. The inhibitory effect of high-perfusion pressure on renin secretion was attenuated by the calcium entry blocker verapamil but not by nifedipine. Thus, if voltage-dependent calcium channels in the juxtaglomerular cell membrane participate in the regulation of renin release then these channels appear to be very insensitive to blockade or augmentation by 1,4-dihydropyridines.

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钙通道激动剂对灌注大鼠肾脏肾素释放的影响。
研究了钙通道激动剂BAY K-8644对灌注大鼠肾脏肾素释放和肾功能的影响。BAY K-8644以剂量依赖的方式增加肾血管阻力,降低肾小球滤过率、钠排泄和尿流量。钙通道阻滞剂硝苯地平可预防这些作用。BAY K-8644对肾素基础分泌无显著影响,且不能阻止低灌注压或异丙肾上腺素对肾素的刺激。高灌注压对肾素分泌的抑制作用被钙进入阻滞剂维拉帕米减弱,而硝苯地平没有。因此,如果肾小球旁细胞膜中的电压依赖性钙通道参与肾素释放的调节,那么这些通道似乎对1,4-二氢吡啶的阻断或增强非常不敏感。
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