Jiang C W, Poole-Wilson P A, Collins P
Department of Cardiac Medicine, National Heart and Lung Institute, London, United Kingdom.
Cardiovasc Res. 1991 Nov;25(11):930-5. doi: 10.1093/cvr/25.11.930.
The purpose was to assess the role of ATP sensitive potassium channels (KATP) in endothelium dependent vasodilatation induced by acetylcholine, or endothelium independent vasodilatation induced by lemakalim in rabbit coronary arteries.
The effect of glibenclamide, a specific inhibitor of KATP, on coronary artery relaxation induced by acetylcholine or lemakalim was investigated. The relaxing effectiveness of acetylcholine and lemakalim on coronary arteries precontracted with KCl (K+) or prostaglandin F2 alpha (PGF2 alpha) was compared.
Left epicardial coronary arteries from male New Zealand white rabbits (2.5-3.0 kg), killed by an overdose of pentobarbitone, were dissected free of connective tissue. Rings suspended in organ baths for the measurement of isometric tension.
K+ (30 mmol.litre-1) and PGF2 alpha (3 mumols.litre-1) caused comparable contraction (p greater than 0.05) in endothelium intact or endothelium denuded coronary arterial rings. Acetylcholine induced relaxation was greater in endothelium intact rings precontracted with PGF2 alpha than with K+ and was abolished by the removal of endothelium. Relaxations induced by acetylcholine (0.1 and 0.3 mumol.litre-1) were reduced from 82(SEM 2.7)% and 93(2.8)% to 71(2.4)% and 82(2.7)% (p less than 0.05), and to 63(3.2)% and 79(4.5)% (p less than 0.05 or less than 0.01) by glibenclamide (3 and 10 mumols.litre-1) respectively in PGF2 alpha precontracted rings; and also attenuated (p less than 0.05 or less than 0.01) in K+ precontracted rings. Lemakalim induced relaxation was greater in endothelium denuded rings precontracted with PGF2 alpha than with K+, and was markedly reduced by glibenclamide (p less than 0.01).
These results suggest that activation of KATP may partially be involved in endothelium dependent relaxation induced by acetylcholine in rabbit coronary arteries. Lemakalim-induced endothelium independent relaxation results mainly from activation of KATP.
本研究旨在评估三磷酸腺苷敏感性钾通道（KATP）在乙酰胆碱诱导的兔冠状动脉内皮依赖性血管舒张或雷马卡林诱导的非内皮依赖性血管舒张中的作用。
研究了KATP特异性抑制剂格列本脲对乙酰胆碱或雷马卡林诱导的冠状动脉舒张的影响。比较了乙酰胆碱和雷马卡林对用氯化钾（K+）或前列腺素F2α（PGF2α）预收缩的冠状动脉的舒张效果。
过量戊巴比妥钠处死的雄性新西兰白兔（2.5 - 3.0千克）的左心外膜冠状动脉，剥离结缔组织。将血管环悬挂于器官浴槽中以测量等长张力。
在完整内皮或去内皮的冠状动脉环中，K+（30 mmol·L-1）和PGF2α（3 μmol·L-1）引起的收缩程度相当（p>0.05）。乙酰胆碱诱导的舒张在PGF2α预收缩的完整内皮环中比在K+预收缩的环中更大，并且去除内皮后舒张消失。在PGF2α预收缩的环中，乙酰胆碱（0.1和0.3 μmol·L-1）诱导的舒张分别从82（标准误2.7）%和93（2.8）%降至71（2.4）%和82（2.7）%（p<0.05），以及降至63（3.2）%和79（4.5）%（p<0.05或<0.01），这是分别加入格列本脲（3和10 μmol·L-1）所致；在K+预收缩的环中舒张也减弱（p<0.05或<0.01）。雷马卡林诱导的舒张在PGF2α预收缩的去内皮环中比在K+预收缩的环中更大，并且被格列本脲显著降低（p<0.01）。
这些结果表明，KATP的激活可能部分参与了兔冠状动脉中乙酰胆碱诱导的内皮依赖性舒张。雷马卡林诱导的非内皮依赖性舒张主要源于KATP的激活。
