Insulin and Insulin-like Growth Factor-I Cause Coronary Vasorelaxation In Vitro

Insulin and insulin-like growth factor-I (IGF-I) may play a role in the modulation of coronary artery tone, yet there are few data regarding their vasoactive effects on the coronary vascular bed. We evaluated the vasorelaxation effects of insulin and IGF-I on porcine coronary epicardial vessels in v...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1998-08, Vol.32 (2), p.228-234
Main Authors: Hasdai, David, Rizza, Robert A, Holmes, David R, Richardson, Darcy M, Cohen, Pinchas, Lerman, Amir
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Coronary Vessels - physiology
Culture Techniques
Endothelium, Vascular - physiopathology
Enzyme Inhibitors - pharmacology
Fundamental and applied biological sciences. Psychology
Heart
Hypoglycemic Agents - pharmacology
Insulin - pharmacology
Insulin-Like Growth Factor I - pharmacology
Nitric Oxide - physiology
Nitric Oxide Synthase - antagonists & inhibitors
omega-N-Methylarginine - pharmacology
Swine
Vasodilation - drug effects
Vasodilation - physiology
Vertebrates: cardiovascular system
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Summary:Insulin and insulin-like growth factor-I (IGF-I) may play a role in the modulation of coronary artery tone, yet there are few data regarding their vasoactive effects on the coronary vascular bed. We evaluated the vasorelaxation effects of insulin and IGF-I on porcine coronary epicardial vessels in vitro and elucidated possible mechanisms. Porcine epicardial arteries were contracted with 10 mol/L endothelin-1 and relaxed with cumulative concentrations of either insulin or IGF-I (10 to 10 mol/L). The above experiments were repeated in vessels without endothelium. Vessels were also incubated with the nitric oxide synthase inhibitor N (L-NMMA; 10 mol/L) with and without 10.5 mol/L L-arginine, the potassium channel blocker tetraethylammonium (TEA; 10 mol/L), and the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-alpha]quinoxalin-1-one (ODQ; 10.5 mol/L); vessels were then contracted with endothelin-1 and relaxed with insulin or IGF-I. Insulin and IGF-I were also added after contraction with 60 mmol/L KCl. Insulin and IGF-I caused a similar decrease in coronary epicardial tension after contraction with endothelin-1 (relaxation of 28 +/- 4% [n=7] and 25 +/- 3% [n=8] with insulin and IGF-I, respectively; P
ISSN:0194-911X
1524-4563
DOI:10.1161/01.hyp.32.2.228