Inwardly rectifying potassium channels in the regulation of vascular tone

被引:34
作者
Chrissobolis, S [1 ]
Sobey, CG [1 ]
机构
[1] Univ Melbourne, Dept Pharmacol, Parkville, Vic 3010, Australia
关键词
potassium channels; inwardly rectifying potassium channels; vasodilatation; artery tone; blood flow; hyperpolarization; potassium; protein kinase C; endothelium-derived hyperpolarizing factor; cardiovascular disease;
D O I
10.2174/1389450033491046
中图分类号
R9 [药学];
学科分类号
1007 [药学];
摘要
Potassium ion (K+) channel activity is one of the major determinants of vascular muscle cell membrane potential and thus vascular tone. Four types of K+ channels are functionally important in the vasculature - Ca2+ activated K+ (K-Ca) channels, voltage-dependent K+ (K-V) channels, ATP-sensitive K+ (K-ATP) channels, and inwardly rectifying K+ (K-IR) channels, and the latter type will be the subject of this review. Recent advances in vascular K-IR channel research indicate that this channel: 1) is present in vascular muscle; 2) modulates basal arterial tone; 3) mediates powerful hyperpolarization and vasodilator responses to small but physiological increases in extracellular K+; 4) may contribute to vasodilatation in response to flow-induced shear stress; 5) may be inhibited by protein kinase C activity; 6) may be involved in vasorelaxation mediated by endothelium-derived hyperpolarizing factor; and 7) may be functionally altered in cardiovascular diseases. Vascular effects of K-IR channels have so far been most extensively studied in the cerebral circulation where K-IR function may be important in coupling cerebral metabolism and blood flow.
引用
收藏
页码:281 / 289
页数:9
相关论文
共 95 条
[1]
Effects of inhibitors of small- and intermediate-conductance calcium-activated potassium channels, inwardly-rectifying potassium channels and Na+/K+ ATPase on EDHF relaxations in the rat hepatic artery [J].
Andersson, DA ;
Zygmunt, PM ;
Movahed, P ;
Andersson, TLG ;
Högestätt, ED .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 129 (07) :1490-1496
[2]
Direct block of native and cloned (Kir2.1) inward rectifier K+ channels by chloroethylclonidine [J].
Barrett-Jolley, R ;
Dart, C ;
Standen, NB .
BRITISH JOURNAL OF PHARMACOLOGY, 1999, 128 (03) :760-766
[3]
Relationship between inward rectifier potassium current impairment and brain injury after cerebral ischemia/reperfusion [J].
Bastide, M ;
Bordet, R ;
Pu, Q ;
Robin, E ;
Puisieux, F ;
Dupuis, B .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (12) :1309-1315
[4]
CHANGES IN RENAL HEMODYNAMICS AND ELECTROLYTE EXCRETION DURING ACUTE HYPERKALEMIA IN CONSCIOUS ADRENALECTOMIZED SHEEP [J].
BEAL, AM ;
BUDTZOLSEN, OE ;
CLARK, RC ;
CROSS, RB ;
FRENCH, TJ .
QUARTERLY JOURNAL OF EXPERIMENTAL PHYSIOLOGY AND COGNATE MEDICAL SCIENCES, 1975, 60 (03) :207-221
[5]
An evaluation of potassium ions as endothelium-derived hyperpolarizing factor in porcine coronary arteries [J].
Bény, JL ;
Schaad, O .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 131 (05) :965-973
[6]
Vasoconstrictors inhibit ATP-sensitive K+ channels in arterial smooth muscle through protein kinase C [J].
Bonev, AD ;
Nelson, MT .
JOURNAL OF GENERAL PHYSIOLOGY, 1996, 108 (04) :315-323
[7]
Kir2.1. encodes the inward rectifier potassium channel in rat arterial smooth muscle cells [J].
Bradley, KK ;
Jaggar, JH ;
Bonev, AD ;
Heppner, TJ ;
Flynn, ERM ;
Nelson, MT ;
Horowitz, B .
JOURNAL OF PHYSIOLOGY-LONDON, 1999, 515 (03) :639-651
[8]
ISOLATION OF NITRIC-OXIDE SYNTHETASE, A CALMODULIN-REQUIRING ENZYME [J].
BREDT, DS ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (02) :682-685
[9]
STUDIES ON POTASSIUM INDUCED CORONARY DILATION IN ISOLATED GUINEA-PIG HEART [J].
BUNGER, R ;
HADDY, FJ ;
QUERENGASSER, A ;
GERLACH, E .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1976, 363 (01) :27-31
[10]
BUSIJA DW, 1992, AM J PHYSIOL, V263, pH1455, DOI 10.1152/ajpheart.1992.263.5.H1455