SEINO, M., ABE, K., ITO, S., YASUJIMA, M., CHIBA, S., HIWATARI, M., SATO, K., GOTO, T., OMATA, K., TAJIMA, J., TANNO, M. and YOSHINAGA, K.
Effects of Nifedipine on Renal Vascular Responses to Vasoactive Agents in Rabbits. Tohoku J. exp. Med., 1984,
142 (1), 67-76-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 E
2). 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 (50μg/kg), decreases in renal blood flow in response to angiotensin II infused at rates of 2.5, 5 and 10ng/kg/min were attenuated by 64% (
p<0.01), 45% (
p<0.05) and 42% (
p<0.05), respectively. Decreases in renal blood flow in response to vasopressin infused at rates of 10, 20 and 50mU/kg/min were also attenuated by nifedipine, 50% (
p<0.05), 57% (
p< 0.05) and 38% (
p<0.05), respectively. However, renal vasoconstrictor responses to norepinephrine (25, 50 and 100ng/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 10ng/kg/min) and prostaglandin E
2 (20, 50 and 100ng/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 E
2 is not altered by nifedipine in anesthetized rabbits.
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