Ogawa N, Ono H
Naunyn Schmiedebergs Arch Pharmacol. 1987 Feb;335(2):189-93. doi: 10.1007/BF00177722.
The role of Ca channel and extracellular Ca2+ on autoregulation of renal blood flow was investigated in the perfused kidney of the anesthetized dog. The perfusion pressure was changed in the range between 60 and 200 mm Hg. Intra-arterial infusion of nifedipine (5 micrograms/min) increased renal blood flow at a perfusion pressure above 100 mm Hg and inhibited autoregulation. Simultaneous infusion of 5 micrograms/min of BAY K 8644 antagonized the effect of nifedipine. Renal blood flow was increased and autoregulatory relationship between flow and perfusion pressure was inhibited by EDTA (30 mg/min) infusion. The inhibitory effect of EDTA on renal autoregulation was counteracted by simultaneous infusion of CaCl2 at 30 mg/min, but not counteracted by that of BAY K 8644 (5 micrograms/min). BAY K 8644 also could not antagonize the inhibitory effect of a vasodilator, papaverine (5 mg/min) on renal blood flow autoregulation. These results provide the evidence that the renal autoregulation involves the process of Ca2+ influx into the vascular smooth muscle cell through the Ca channels.
在麻醉犬的灌注肾中研究了钙通道和细胞外钙离子对肾血流自身调节的作用。灌注压力在60至200毫米汞柱之间变化。在灌注压力高于100毫米汞柱时，动脉内输注硝苯地平（5微克/分钟）可增加肾血流并抑制自身调节。同时输注5微克/分钟的BAY K 8644可拮抗硝苯地平的作用。输注乙二胺四乙酸（EDTA，30毫克/分钟）可增加肾血流，并抑制血流与灌注压力之间的自身调节关系。同时输注30毫克/分钟的氯化钙可抵消EDTA对肾自身调节的抑制作用，但输注5微克/分钟的BAY K 8644则不能抵消。BAY K 8644也不能拮抗血管扩张剂罂粟碱（5毫克/分钟）对肾血流自身调节的抑制作用。这些结果证明，肾自身调节涉及钙离子通过钙通道流入血管平滑肌细胞的过程。
