Seino M, Abe K, Ito S, Yasujima M, Chiba S, Hiwatari M, Sato K, Goto T, Omata K, Tajima J
Tohoku J Exp Med. 1984 Jan;142(1):67-76. doi: 10.1620/tjem.142.67.
The present study was designed to investigate the effects of the Ca-antagonist, nifedipine, on receptor-mediated renal vascular responses to vasoconstrictors (angiotensin II, norepinephrine and vasopressin) and vasodilators (bradykinin and prostaglandin E2). Renal blood flow was estimated by noncannulating electromagnetic flowmetry in anesthetized rabbits. Vasoactive substances were infused directly into the renal artery. After the intravenous administration of nifedipine (50 micrograms/kg), decreases in renal blood flow in response to angiotensin II infused at rates of 2.5, 5 and 10 ng/kg/min were attenuated by 64% (p less than 0.01), 45% (p less than 0.05) and 42% (p less than 0.05), respectively. Decreases in renal blood flow in response to vasopressin infused at rates of 10, 20 and 50 mU/kg/min were also attenuated by nifedipine, 50% (p less than 0.05), 57% (p less than 0.05) and 38% (p less than 0.05), respectively. However, renal vasoconstrictor responses to norepinephrine (25, 50 and 100 ng/kg/min) did not change significantly after the administration of nifedipine. Increases in renal blood flow induced by the intrarenal infusion of bradykinin (2.5, 5 and 10 ng/kg/min) and prostaglandin E2 (20, 50 and 100 ng/kg/min) were not affected by nifedipine. These results suggest that receptor-mediated vasoconstrictor responses of the renal vascular bed to angiotensin II and vasopressin are produced mainly by Ca++ influx but that of norepinephrine is not. Furthermore, it is confirmed that the renal vasodilator effect of bradykinin and prostaglandin E2 is not altered by nifedipine in anesthetized rabbits.
本研究旨在探讨钙拮抗剂硝苯地平对受体介导的肾血管对血管收缩剂（血管紧张素 II、去甲肾上腺素和血管加压素）和血管扩张剂（缓激肽和前列腺素 E2）的反应的影响。通过非插管电磁血流测定法在麻醉兔中估计肾血流量。将血管活性物质直接注入肾动脉。静脉注射硝苯地平（50 微克/千克）后，以 2.5、5 和 10 纳克/千克/分钟的速率注入血管紧张素 II 时，肾血流量的减少分别被减弱了 64%（p < 0.01）、45%（p < 0.05）和 42%（p < 0.05）。以 10、20 和 50 毫单位/千克/分钟的速率注入血管加压素时，肾血流量的减少也被硝苯地平减弱，分别为 50%（p < 0.05）、57%（p < 0.05）和 38%（p < 0.05）。然而，注射硝苯地平后，肾血管对去甲肾上腺素（25、50 和 100 纳克/千克/分钟）的收缩反应没有显著变化。肾内注入缓激肽（2.5、5 和 10 纳克/千克/分钟）和前列腺素 E2（20、50 和 100 纳克/千克/分钟）引起的肾血流量增加不受硝苯地平影响。这些结果表明，肾血管床对血管紧张素 II 和血管加压素的受体介导的血管收缩反应主要由 Ca++内流产生，而去甲肾上腺素的则不是。此外，证实了在麻醉兔中，缓激肽和前列腺素 E2 的肾血管扩张作用不受硝苯地平影响。
