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 μg/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<0.01), 45% (p<0.05) and 42% <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<0.05), 57% (p< 0.05) and 38% (p<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.-angiotensin II ; norepinephrine ; vasopressin ; bradykinin ; prostaglandin E2.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)