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Titolo:
Potassium channel function in vascular disease
Autore:
Sobey, CG;
Indirizzi:
Univ Melbourne, Dept Pharmacol, Parkville, Vic 3010, Australia Univ Melbourne Parkville Vic Australia 3010 arkville, Vic 3010, Australia
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 1, volume: 21, anno: 2001,
pagine: 28 - 38
SICI:
1079-5642(200101)21:1<28:PCFIVD>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; SMOOTH-MUSCLE CELLS; SENSITIVE K+ CHANNELS; GENE-RELATED PEPTIDE; ENDOTHELIUM-DEPENDENT RELAXATION; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; PORCINE CORONARY-ARTERY; RABBIT BASILAR ARTERY; NITRO-L-ARGININE; CEREBRAL VASOSPASM;
Keywords:
hypertension; depolarization; endothelium-derived hyperpolarizing factor; hypercholesterolemia; hyperpolarization;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
151
Recensione:
Indirizzi per estratti:
Indirizzo: Sobey, CG Univ Melbourne, Dept Pharmacol, Parkville, Vic 3010, Australia Univ Melbourne Parkville Vic Australia 3010 Vic 3010, Australia
Citazione:
C.G. Sobey, "Potassium channel function in vascular disease", ART THROM V, 21(1), 2001, pp. 28-38

Abstract

Potassium ion (K+) channel activity is a major regulator of vascular muscle cell membrane potential (E-m) and is therefore an important determinant of vascular tone. There is growing evidence that the function of several types of vascular K+ channels is altered during major cardiovascular diseases,such as chronic hypertension, diabetes, and atherosclerosis. Vasoconstriction and the compromised ability of an artery to dilate are likely consequences of defective K+ channel function in blood vessels during these disease states. In some instances, increased K+ channel function mag help to compensate for increased vascular tone. Endothelial cell dysfunction is commonly associated with cardiovascular disease, and altered activity of nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor could also contribute to changes in resting K+ channel activity, E-m, and K+ channel-mediated vasodilatation. Our current knowledge of the effects of disease on vascular K+ channel function almost exclusively relies on interpretation ofdata obtained by using pharmacological modulators of K+ channels. As further progress is made in the development of more selective drugs and through molecular approaches such as gene targeting technology in mice, specific Kchannel abnormalities and their causes in particular diseases should be more readily identified, providing novel directions for vascular therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 18:57:35