L-arginine-induced dilatation of goat coronary artery involves activation of KATP channels

被引:2
|
作者
Deka, Dilip K. [1 ]
Mishra, Santosh K. [2 ]
Raviprakash, Vellanki [2 ]
机构
[1] AAU, Dept Pharmacol & Toxicol, Khanapara 781022, Guwahati, India
[2] IVRI, Div Pharmacol, Izatnagar 243122, Bareilly, India
关键词
Coronary artery; Vasodilatation; K-ATP channel; L-arginine; ENDOTHELIUM-DEPENDENT RELAXATION; NITRIC-OXIDE; POTASSIUM CHANNELS; RELAXING FACTOR; SMOOTH-MUSCLE; RAT; MODULATION; PRECURSOR; RESPONSES; ANALOGS;
D O I
10.1016/j.ejphar.2009.03.031
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In the present study, the mechanism of relaxant response of nitric oxide precursor, L-arginine, was investigated in goat isolated coronary artery. L-arginine (I mM) reversed the U-46619 (1 mu M)-induced contraction both in endothelium-intact and endothelium-denuded arterial ring preparations. L-arginine analogues, L-NAME, L-NNA and L-NMMA and the guanylyl cyclase inhibitor, methylene blue failed to attenuate the relaxant response of L-arginine. These observations negate the involvement of nitric oxide in mediating the relaxation by L-arginine. K-ATP channel blocker, glibenclamide (3 mu M), abolished the vasorelaxant responses Of L-arginine in endothelium-denuded preparations, thereby suggesting the involvement of K-ATP channels. Further, L-arginine also failed to induce relaxation of the coronary arterial rings constricted with K+ (80 mM)-PSS. Taken together, the results of the present study suggest that L-arginine relaxes goat isolated coronary artery through activation of K-ATP channels. (C) 2009 Elsevier B.V. All rights reserved
引用
收藏
页码:113 / 117
页数:5
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