Ogawa N, Yokota S, Ono H
Department of Pharmacology and Toxicology, Hatano Research Institute, Food and Drug Safety Center, Kanagawa, Japan.
J Cardiovasc Pharmacol. 1988 Feb;11(2):147-50.
The effect of bepridil and diltiazem on autoregulation of renal blood flow was examined in connection with interaction of BAY K 8644 in perfused kidney of anesthetized dogs. When the perfusion pressure was changed stepwise over the range between 60 and 200 mm Hg, renal blood flow remained nearly constant between 100 and 200 mm Hg. Intra-arterial infusion of diltiazem (50 microgram/min) or bepridil (1 mg/min) increased renal blood flow at perfusion pressure above 100 mm Hg and completely inhibited renal autoregulation. Simultaneous infusion of 5 microgram/min of BAY K 8644 with diltiazem antagonized both the increase of renal blood flow and the impairment of autoregulation, whereas simultaneous infusion of BAY K 8644 (5 micrograms/min) could not block the impairment of renal autoregulation induced by bepridil. These results show that the inhibitory effect of bepridil on autoregulation of renal blood flow is due to some mechanism other than Ca channel blocking action in renal vasculature.
在麻醉犬的灌注肾中,结合BAY K 8644的相互作用,研究了苄普地尔和地尔硫䓬对肾血流自动调节的影响。当灌注压力在60至200 mmHg之间逐步变化时,肾血流在100至200 mmHg之间保持几乎恒定。动脉内输注地尔硫䓬(50微克/分钟)或苄普地尔(1毫克/分钟)在灌注压力高于100 mmHg时增加肾血流,并完全抑制肾自动调节。同时输注5微克/分钟的BAY K 8644与地尔硫䓬可拮抗肾血流增加和自动调节受损,而同时输注BAY K 8644(5微克/分钟)不能阻断苄普地尔诱导的肾自动调节受损。这些结果表明,苄普地尔对肾血流自动调节的抑制作用是由于肾血管中钙通道阻断作用以外的某种机制。