The role of ATP-sensitive potassium channels in regulating coronary microcirculation

Biorheology ◽  
1993 ◽  
Vol 30 (5-6) ◽  
pp. 371-380 ◽  
Author(s):  
T. Komaru ◽  
H. Kanatsuka ◽  
K. Dellsperger ◽  
T. Takishima
1999 ◽  
Vol 277 (3) ◽  
pp. H1252-H1259 ◽  
Author(s):  
Yasuhiro Nishikawa ◽  
David W. Stepp ◽  
William M. Chilian

Responses of epicardial coronary arterioles to ACh were measured using stroboscopic fluorescence microangiography in dogs ( n = 38). ACh (0.1 and 0.5 μg ⋅ kg−1 ⋅ min−1ic) dilated small (<100 μm, 11 ± 2 and 19 ± 2%, respectively) and large (>100 μm, 6 ± 3 and 13 ± 3%, respectively) arterioles at baseline. Combined administration of N ω-monomethyl-l-arginine (l-NMMA; 1.0 μmol/min ic) and indomethacin (10 mg/kg iv) eliminated ACh-induced dilation in large coronary arterioles but only partially attenuated that in small arterioles. Suffusion of a buffer containing 60 mM KCl (high KCl) completely abolished cromakalim-induced dilation in arterioles and in combination with l-NMMA plus indomethacin completely blocked ACh-induced dilation in small arterioles. This indicated that the vasodilation to ACh that persists in small arterioles after administration of l-NMMA and indomethacin is mediated via a hyperpolarizing factor. The ACh-induced vasodilation remaining after l-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes. These observations are consistent with the view that endothelium-derived hyperpolarizing factor (EDHF) is a product of cytochrome P-450 enzymes and produces vasodilation by the opening of large-conductance potassium channels. We conclude that ACh-induced dilation in large coronary arterioles is mediated mainly by nitric oxide (NO), whereas, in small arterioles both NO and EDHF mediate dilation to ACh. These data provide the first direct evidence for an in vivo role of EDHF in small coronary arterioles.


2009 ◽  
Vol 3 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Tsuneo Ogawa ◽  
Monica Forero ◽  
Patrick G. Burgon ◽  
Mercedes L. Kuroski de Bold ◽  
Tina Georgalis ◽  
...  

2008 ◽  
Vol 104 (4) ◽  
pp. 914-925 ◽  
Author(s):  
Beatriz Goñi-Allo ◽  
Elena Puerta ◽  
María Ramos ◽  
Berta Lasheras ◽  
Joaquín Jordán ◽  
...  
Keyword(s):  

2011 ◽  
Vol 3 (1) ◽  
pp. 113-124
Author(s):  
Lia Crotti ◽  
Roberto Insolia ◽  
Peter J. Schwartz

2015 ◽  
Vol 119 ◽  
pp. 73-79 ◽  
Author(s):  
Xiang-Yao Li ◽  
Hiroki Toyoda
Keyword(s):  

1998 ◽  
Vol 78 (1) ◽  
pp. 53-97 ◽  
Author(s):  
FRANK M. FARACI ◽  
DONALD D. HEISTAD

Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.


2002 ◽  
Vol 34 (6) ◽  
pp. A10
Author(s):  
Péter Biliczki ◽  
László Virág ◽  
Norbert Iost ◽  
Julius Gy. Papp ◽  
András Varró

1995 ◽  
Vol 108 (3) ◽  
pp. 1161-1170 ◽  
Author(s):  
N. Ilan ◽  
N. Moran ◽  
A. Schwartz

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