Calcium-activated potassium channels in the endothelium of intact rat aorta

被引:115
作者
Marchenko, SM [1 ]
Sage, SO [1 ]
机构
[1] UNIV CAMBRIDGE,PHYSIOL LAB,CAMBRIDGE CB2 3EG,ENGLAND
来源
JOURNAL OF PHYSIOLOGY-LONDON | 1996年 / 492卷 / 01期
基金
英国惠康基金;
关键词
D O I
10.1113/jphysiol.1996.sp021288
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
1. Single K+ channel currents and membrane potential were recorded in the endothelium of excised intact rat aorta. 2. Two types of K+ channel were found in excised patches, K-Ch and K-Ap. With Na+ and K+ as the main external and internal cations, outward conductances were 6.7 pS (K-Ch) and 2.8 pS (K-Ap). In symmetric 150 mar K+, the inward conductances were 18 and 9.1 pS. 3. Activation by Ca2+ was concentration dependent. K-Ch channels were activated by [Ca2+] > 0.1 mu M and K-Ap by [Ca2+] > 0.5 mu M. 4. Apamin at concentrations > 1 nM inhibited K-Ap channels. Block was complete at 10 nM. K-Ap channels were insensitive to charybdotoxin. K-Ch channels were inhibited by Ii charybdotoxin at concentrations > 50 nM, but were insensitive to apamin. 5. d-Tubocurarine (dTC) evoked flickering activity of K-Ap channels at concentrations > 5 mu M and complete block at 100 mu M. At these doses, dTC did not affect K-Ch channels, but at concentrations > 1 mM it decreased the single channel amplitude. 6. Hyperpolarization evoked by acetylcholine was unaffected by apamin or dTC at low concentrations (less than or equal to 100 mu M), but inhibited by high concentrations of charybdotoxin (> 50 nM) or dTC (> 1 mM). 7. These data suggest that K-Ch channels are novel Ca2+-activated K+ channels responsible for the ACh-evoked hyper polarization in the endothelium of rat aorta.
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页码:53 / 60
页数:8
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