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Am J Physiol Heart Circ Physiol 284: H1080-H1086, 2003. First published December 19, 2002; doi:10.1152/ajpheart.00465.2002
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Vol. 284, Issue 4, H1080-H1086, April 2003

Mechanism of thrombin-induced vasodilation in human coronary arterioles

John J. Bosnjak1, Ken Terata1, Hiroto Miura1, Atsushi Sato1, Alfred C. Nicolosi2, Monica McDonald3, Sara A. Manthei1, Takashi Saito4, Ossama A. Hatoum1, and David D. Gutterman1

1 Medical College of Wisconsin, Cardiovascular Center, 2 Veterans Affairs Medical Center, and 3 Midwest Heart Surgery Institute, Milwaukee, Wisconsin 53226; and 4 Second Department of Internal Medicine, Akita University, Akita City 0108543, Japan

Thrombin (Thromb), activated as part of the clotting cascade, dilates conduit arteries through an endothelial pertussis toxin (PTX)-sensitive G-protein receptor and releases nitric oxide (NO). Thromb also acts on downstream microvessels. Therefore, we examined whether Thromb dilates human coronary arterioles (HCA). HCA from right atrial appendages were constricted by 30-50% with endothelin-1. Dilation to Thromb (10-4-1 U/ml) was assessed before and after inhibitors with videomicroscopy. There was no tachyphylaxis to Thromb dilation (maximum dilation = 87.0%, ED50 = 1.49 × 10-2). Dilation to Thromb was abolished with either hirudin or denudation but was not affected by PTX. Neither Nomega -nitro-L-arginine methyl ester (n = 7), indomethacin (n = 9), 1H-[1,2,4] oxadiazolo-[4,3-a]quinoxalin-1-one (n = 6), tetraethylammonium chloride (n = 5), nor iberiotoxin (n = 4) reduced dilation to Thromb. However, KCl (maximum dilation = 89 ± 5 vs. 20 ± 10%; P < 0.05; n = 7), tetrabutylammonium chloride (maximum dilation = 79 ± 7 vs. 21 ± 4%; P < 0.05; n = 5), and charybdotoxin (maximum dilation = 89 ± 4 vs. 10 ± 2%; P < 0.05; n = 4) attenuated dilation to Thromb. In contrast to animal models, Thromb-induced dilation in human arterioles is independent of Gi-protein activation and NO release. However, Thromb dilation is endothelium dependent, is maintained on consecutive applications, and involves activation of K+ channels. We speculate that an endothelium-derived hyperpolarizing factor contributes to Thromb-induced dilation in HCA.

coronary circulation; coronary disease; K+ channel; vasoactive agent


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