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Functional evidence for up‐regulated angiotensin converting enzyme (ACE) in coronary arterioles of rats on high fat diet
Author(s) -
Feher Attila,
Beleznai Timea,
Labinskyy Nazar,
Bagi Zsolt
Publication year - 2010
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.24.1_supplement.1034.9
Subject(s) - bradykinin , captopril , medicine , vasodilation , endocrinology , angiotensin converting enzyme , coronary arteries , arteriole , ace inhibitor , coronary vasodilator , coronary atherosclerosis , angiotensin ii , microcirculation , blood pressure , artery , coronary artery disease , receptor
Angiotensin converting enzyme (ACE) inhibitors prevent cardiovascular complications in cardiovascular diseases. We hypothesized that ACE, expressed in the wall of coronary resistance arteries is up‐regulated in obesity, which has an impact on regulation of coronary arteriolar diameter. In isolated, pressurized coronary arterioles (≈ 100 μm) angiotensin II (Ang II) elicited dilations that were not different between control (male Wistar rats on normal diet) and obese rats (male Wistar rats fed a 60% fat containing diet for 12 weeks). Dilations to Ang I, however, were significantly enhanced in coronary arterioles of obese rats, when compared to controls (64±7 vs. 20±4 %). Moreover, bradykinin elicited constriction in coronary vessels of obese rats (−9±6 %), whereas it dilated vessels in control animals (24±65). In the presence of the ACE inhibitor, captopril (10 μM), coronary dilations to Ang I were similar in the two groups (8±6 vs. 5±3 %). Whereas captopril restored dilations to bradykinin in obese rats (to 15±10 %), but it did not affect control responses (32±12 %). Collectively, we provide functional evidence for up‐regulated ACE in the coronary microvascular wall in obese rats fed a high fat diet. Up‐regulation of ACE is responsible for diminished dilation to bradykinin, that can be restored by ACE inhibition to enhance vasodilation of coronary arterioles in obesity. (AHA 0735540T and NIH NHLBI 43023)