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Endothelium‐dependent dilation in coronary arterioles following chronic nitric oxide synthase inhibition
Author(s) -
Laughlin Maurice Harold,
Thorne P K,
McAllister R M
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a270-b
Subject(s) - bradykinin , sodium nitroprusside , nitric oxide , endothelium , medicine , vasomotor , vasodilation , nitric oxide synthase , chemistry , dilation (metric space) , endocrinology , arteriole , cardiology , microcirculation , mathematics , combinatorics , receptor
This study tested the hypothesis that chronic inhibition of NOS with N G ‐nitro‐L‐arginine methyl ester (L‐NAME) decreases endothelium‐dependent dilation due to decreased NO release. Vasomotor reactivity of coronary arterioles isolated from 8 swine that were chronically administered L‐NAME (8.3 ± 0.5 mg/kg/d) in their water for 30–90 days and 7 controls was examined. Arterioles isolated from the left ventricular apex were mounted on glass micropipettes and allowed to develop spontaneous tone. Dilation was produced by increasing doses of endothelium‐dependent bradykinin (BK) and –independent sodium nitroprusside (SNP), performed in the presence and absence of L‐NAME [300μM] in the bath. The relative contribution of NO release to the dilation was assessed by comparing dilation between arterioles with and without acute L‐NAME treatment. BK and SNP dilation was similar in both groups. However, the relative contribution of NO release to BK‐induced dilation (3 x 10 −10 M, BK) was significantly decreased in the arterioles from pigs chronically treated with L‐NAME (24±12 %) compared to arterioles from control pigs (62±11 %). These results suggest that endothelium‐dependent dilation is maintained in coronary arterioles following chronic L‐NAME inhibition of NOS activity, perhaps by compensatory increases in the release of non‐NOS mediators. (NIH Grant #s RR‐18276 and HL‐52490).