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Release of nitric oxide by angiotensin‐(1–7) from porcine coronary endothelium: implications for a novel angiotensin receptor
Author(s) -
Pörsti Ilkka,
Bara Agnieszka T.,
Busse Rudi,
Hecker Markus
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb14787.x
Subject(s) - dilator , angiotensin ii , nitric oxide , medicine , chemistry , endocrinology , nitric oxide synthase , endothelium , receptor , receptor antagonist , angiotensin ii receptor type 1 , renin–angiotensin system , valsartan , angiotensin converting enzyme , pharmacology , antagonist , blood pressure
The angiotensin I (AI) metabolite, A(1–7), elicited a concentration‐dependent dilator response (ED 50 ≥ 2 μ m ) in porcine coronary artery rings which was markedly attenuated by the nitric oxide (NO) synthase inhibitor, N G ‐nitro‐ l ‐arginine, and abolished after removal of the endothelium. This effect of the heptapeptide was not mimicked by AII, AIII or A(3–8) at comparable concentrations. The A(1–7)‐induced relaxation was not affected by AT 1 or AT 2 receptor blockade or cyclo‐oxygenase inhibition, but was attenuated by the B 2 receptor antagonist, Hoe 140, and augmented by the angiotensin‐converting enzyme (ACE) inhibitor, quinaprilat. These findings suggest that the relaxation to A(1–7) was mediated by the release of NO from the coronary endothelium through activation of an, as yet unidentified, AT receptor, the occupation of which also seems to stimulate the release of vasoactive kinins. Since A(1–7) accumulates during ACE inhibition, this mechanism may contribute to the coronary dilator effect of ACE inhibitors in vivo .