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Multiple effects of diabetes mellitus on the vasomotor responses of human coronary arterioles
Author(s) -
Bagi Zsolt,
Erdei Nora,
Szerafin Tamas,
Edes Istvan,
Koller Akos
Publication year - 2007
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.21.6.a1226-b
Subject(s) - dilator , bradykinin , medicine , vasodilation , endocrinology , diabetes mellitus , sodium nitroprusside , phenylephrine , arteriole , acetylcholine , vasomotor , coronary atherosclerosis , microcirculation , cardiology , chemistry , coronary artery disease , blood pressure , nitric oxide , receptor
In humans, the intrinsic mechanisms regulating coronary arteriolar tone could be affected by diabetes mellitus (DM), which however has not yet been fully elucidated. Thus, we investigated agonist‐induced responses of coronary arterioles obtained from patients (N=25) without (non‐DM) and with DM. In isolated, pressurized (80 mmHg) coronary arterioles (95±15 μm) acetylcholine (ACh) elicited dilations in non‐DM patients (1μM: 82±5%), whereas caused constrictions in arterioles of DM subjects (1μM: −29±7%). In contrast, bradykinin (BK) induced only dilations in both groups, which were greater in arterioles from DM patients (10nM: 77±10%), than in non‐DM (10nM: 38±14%). Dilations to NO‐donor, sodium nitroprusside were not different in the 2 groups. Inhibition of NO synthesis with L‐NAME reduced ACh‐induced dilations in controls but did not affect ACh‐evoked constrictions in DM patients and BK‐induced dilations in both groups. In DM patients enhanced dilations to BK were reduced by the selective cyclooxygenase‐2 (COX‐2) inhibitor, NS‐398; and a marked COX‐2 immunostaining was reveled in coronary arterioles of DM subjects. We conclude that in isolated coronary arterioles from humans with DM, in addition to the impairment of NO‐mediation, a constrictor factor is released to ACh. In contrast, there is an enhanced dilation to BK, which is likely due to the increased release of COX‐2‐derived dilator prostaglandins. Supported by AHA NE Aff. 0555897T and Hungarian NSRF/OTKA ‐T48376 and HSC/ETT 364/2006.