Dietz J R
Ren Physiol. 1986;9(5):279-86. doi: 10.1159/000173092.
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.
在灌注的大鼠肾脏中研究了钙通道激动剂BAY K - 8644对肾素释放和肾功能的影响。BAY K - 8644以剂量依赖性方式增加肾血管阻力并降低肾小球滤过率、钠排泄和尿流量。这些作用可被钙通道阻滞剂硝苯地平阻断。BAY K - 8644对基础肾素分泌无显著影响，且不能阻止低灌注压力或异丙肾上腺素对肾素的刺激。高灌注压力对肾素分泌的抑制作用可被钙内流阻滞剂维拉帕米减弱，但不能被硝苯地平减弱。因此，如果球旁细胞膜上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 - 二氢吡啶类药物的阻断或增强非常不敏感。
