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Influence of the vascular endothelium on angiotensin II‐induced contractions in rabbit renal artery
Author(s) -
Zhang J.,
Pfaffendorf M.,
Zhang JS,
Zwieten PA
Publication year - 1995
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1995.tb00261.x
Subject(s) - renal artery , endothelium , angiotensin ii , rabbit (cipher) , medicine , artery , blood vessel , cardiology , renin–angiotensin system , lagomorpha , endocrinology , anatomy , chemistry , kidney , blood pressure , statistics , mathematics
Summary— The influence of vascular endothelium on angiotensin II‐induced contraction and the underlying mechanisms in the rabbit renal artery were investigated. In endothelium‐intact preparations, angiotensin II (3–100 nM) caused a concentration‐dependent increase in tension by maximally (E max ) 0.74 ± 0.05 g. Removal of the endothelium significantly enhanced the angiotensin II‐induced contractions (E max : 3.91 ± 0.19 g). Indomethacin (10 μM) did not influence the angiotensin II‐induced contractions. Methylene blue (10 μM) and N G ‐methyl‐1‐arginine (L‐NMMA, 5 μM) significantly enhanced angiotensin II‐induced contractions by 418 ± 29% and 200 ± 14%, respectively, in endothelium intact preparations, but not in those devoid of endothelium. L‐arginine (1 mM), but not D‐arginine, reversed the L‐NMMA‐induced enhancement of the angiotensin II‐induced contraction. The present results suggest that angiotensin II‐induced contractions in rabbit renal artery are largely subject to the influence of the endothelium. The endothelium‐derived relaxant factor (EDRF), rather than cyclo‐oxygenase products, appears to be involved in mediating the inhibitory effects of the endothelium. Nitric oxide (NO) derived from endothelium may play a major role in inhibiting angiotensin II‐induced contractions in this preparation.