Ito S, Seino M, Yasujima M, Abe K, Yoshinaga K
Tohoku J Exp Med. 1983 May;140(1):53-8. doi: 10.1620/tjem.140.53.
Effects of a Ca-antagonist, nifedipine, on renal vascular responses and systemic pressor responses to angiotensin II and norepinephrine were studied in anesthetized rabbits. The changes of renal blood flow were estimated by an electromagnetic flowmeter. After the intravenous administration of nifedipine (50 micrograms/kg), mean blood pressure decreased from 116 +/- 3.1 mmHg to 102 +/- 3.4 mmHg (p less than 0.001). Renal vascular responses to angiotensin II were attenuated significantly after the administration of nifedipine, but not changed to norepinephrine. Pressor responses to angiotensin II at a low dose were significantly diminished after the administration of nifedipine (p less than 0.05), whereas it had no effect at higher doses. Nifedipine tended to suppress the increase in arterial pressure induced by norepinephrine, but the changes were not statistically significant. These results suggest that calcium influx in the vascular smooth muscle cells is not likely to be a common pathway in the vasoconstrictor reaction to angiotensin II and norepinephrine in anesthetized rabbit.
在麻醉兔中研究了钙拮抗剂硝苯地平对肾血管反应以及对血管紧张素II和去甲肾上腺素的全身升压反应的影响。肾血流量的变化通过电磁流量计估算。静脉注射硝苯地平（50微克/千克）后，平均血压从116±3.1毫米汞柱降至102±3.4毫米汞柱（p<0.001）。给予硝苯地平后，肾血管对血管紧张素II的反应明显减弱，但对去甲肾上腺素的反应未改变。给予硝苯地平后，低剂量血管紧张素II的升压反应明显减弱（p<0.05），而高剂量时则无影响。硝苯地平倾向于抑制去甲肾上腺素引起的动脉压升高，但变化无统计学意义。这些结果表明，在麻醉兔中，血管平滑肌细胞中的钙内流不太可能是对血管紧张素II和去甲肾上腺素血管收缩反应的共同途径。
