Ogawa N
Department of Pharmacology and Toxicology, Hatano Research Institute, Food and Drug Safety Center, Kanagawa, Japan.
J Pharm Pharmacol. 1990 Feb;42(2):138-40. doi: 10.1111/j.2042-7158.1990.tb05371.x.
The effect of nicardipine, a Ca channel blocker, on autoregulation of renal blood flow and perfusion pressure-vascular resistance relationship has been investigated in perfused kidneys of anaesthetized dogs. In control animals excellent autoregulation of renal blood flow and pressure-dependent elevation of vascular resistance were observed above 100 mmHg of perfusion pressure. However, intra-arterial infusion of nicardipine at doses of 3 and 10 micrograms min-1 showed dose-dependent impairment of the autoregulatory response and of elevation of vascular resistance. Infusion of nicardipine (2.5 micrograms min-1) into the renal artery also inhibited renal vasoconstriction induced by YC-170, a Ca channel activator. These results suggest that the inhibitory effect of nicardipine upon renal autoregulation may be due to its Ca2+ channel blocking action.
在麻醉犬的灌注肾中，研究了钙通道阻滞剂尼卡地平对肾血流自身调节以及灌注压与血管阻力关系的影响。在对照动物中，当灌注压高于100 mmHg时，观察到肾血流有良好的自身调节以及血管阻力随压力依赖性升高。然而，以3和10微克/分钟的剂量动脉内输注尼卡地平显示出自身调节反应和血管阻力升高呈剂量依赖性受损。向肾动脉输注尼卡地平（2.5微克/分钟）也抑制了由钙通道激活剂YC-170诱导的肾血管收缩。这些结果表明，尼卡地平对肾自身调节的抑制作用可能归因于其钙通道阻滞作用。
