Beta-adrenoceptor-mediated release of angiotensin II from mesenteric arteries
- 1 January 1986
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 250 (1), H144-H148
- https://doi.org/10.1152/ajpheart.1986.250.1.h144
Abstract
Essential components of the renin-angiotensin system such as renin enzymes, angiotensinogen, converting enzyme, and angiotensin receptors have been found in vascular tissues. Locally generated angiotension (ANG) II may regulate vascular tone by contracting vascular smooth muscle or potentiating sympathetic activity. Recently it was suggested that .beta.-adrenoceptor-induced enhancement of noradrenergic neurotransmission is mediated by the vascular renin-angiotensin system. The present study was designated to obtain direct evidence for the release of ANG II from the vasculature by .beta.-adrenoceptor activation. Isolated rat mesenteric arteries were perfused in vitro with Krebs-Ringer solution, and released ANG II was concentrated in a Sep-Pak C-18 cartridge connected to the perfusion system. High-pressure liquid chromatography combined with radioimmunoassay clearly demonstrated the presence of ANG I, II, and a small amount of ANG III in the perfusate. Isoproterenol (10-9 -10-6 M) induced the enhancement of pressor responses to nerve stimulation. This effect was markedly suppressed by propranolol (5 .times. 10-7 M), captopril (2 .times. 10-6 M), or [Sar1 -Ile8]ANG II (10-6 M). Isoproterenol (10-9 -10-6 M) caused increase in the release of ANG II from mesenteric arteries. The increase in ANG II release during isoproterenol (10-6 M) infusion was blocked by propranolol (10-6 M). Captopril (2 .times. 10-6 M) also inhibited the increase in ANG II induced by isoproterenol. These results indicate that locally generated ANG II is released from isolated perfused rat mesenteric arteries and its release is mediated by .beta.-adrenoceptors.This publication has 11 references indexed in Scilit:
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