Response of coronary microvascular collaterals to activation of ATP-sensitive K+ channels.
Response of coronary microvascular collaterals to activation of ATP-sensitive K+ channels.
复制标题
冠状动脉微血管侧枝对 ATP 敏感 K 通道激活的反应。
DOI：
10.1016/s0008-6363(97)00112-0
复制
发表时间：
1997
影响因子：
10.8
通讯作者：
Fujii,M
中科院分区：
文献类型：
--
作者：
Lamping,KG;Nuno,DW;Brooks,LA;Fujii,M
Objective:Studies have suggested that collateral vessels of the coronary and hind-limb circulations are more sensitive to activation of ATP-sensitive K+channels than are non-collateral vessels. The objective of the present study was to compare responses of microvascular non-collaterals, native collaterals and stimulated collaterals in the heart to three vasodilators which act through different mechanisms: activation of ATP-sensitive K+channels with aprikalim, release of nitric oxide with acetylcholine, and endothelium-independent activation of soluble guanylate cyclase with nitroglycerin.Methods:Collateral growth was stimulated by placing an Ameroid occluder on the proximal left circumflex artery in dogs. Non-collaterals, native collaterals and stimulated collaterals (100–220 μm in diameter) were isolated, cannulated on micropipettes and pressurized in vitro. Vessel diameters were measured using videomicroscopy.Results:Dilation to aprikalim (10−8–10−5M), acetylcholine (10−9–10−6M) and nitroglycerin (10−8–3×10−4M) were similar in non-collateral, native collateral and stimulated collaterals. Dilation of native collaterals to aprikalim and acetylcholine was attenuated by glibenclamide (10 μM), an inhibitor of ATP-sensitive K+channels, but not by tetraethylammonium (1 mM), a non-selective inhibitor of K+channels. Dilation of native collaterals to acetylcholine but not aprikalim was also inhibited by nitro-l-arginine (10 μM), an inhibitor of nitric oxide synthase.Conclusion:These findings suggest that microvascular native and stimulated collaterals respond to activation of ATP-sensitive K+channels and acetylcholine similar to non-collaterals of similar size. Thus, changes in reactivity of collaterals to activation of ATP-sensitive K+channels are not related to changes in the ability of the vessels to respond to vasodilators but may primarily be determined by a change in the distribution of collateral vessel size.
