Regulation of potassium channels in coronary arterial smooth muscle by endothelium-derived vasodilators

被引:81
作者
Li, PL [1 ]
Zou, AP [1 ]
Campbell, WB [1 ]
机构
[1] MED COLL WISCONSIN,DEPT PHYSIOL,MILWAUKEE,WI 53226
关键词
potassium channels; nitric oxide; prostacyclin; epoxyeicosatrienoic acids; endothelium; coronary artery;
D O I
10.1161/01.HYP.29.1.262
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Recent studies have suggested that coronary endothelial cells produce and release nitric oxide (NO), prostaglandin I-2, and epoxyeicosatrienoic acids (EETs). These endothelium-derived vasodilators play an important role in the control of coronary vascular tone. However, the mechanism by which these endothelium-derived vasodilators cause relaxation of coronary arterial smooth muscle has yet to be determined. This study characterized and compared the effects of NO, prostaglandin I-2, and 11,12-EET on the two main types of potassium Channels in small bovine coronary arterial smooth muscle: the large conductance Ca2+-activated K+ channels (K-Ca) and 4-aminopyridine-sensitive delayed rectifier K+ channels (K-drf) In cell-attached patches, nonoate, an NO donor, activated both K-Ca and K-drf channels. The open probability of both K-Ca and K-drf channels increased 10- to 25-fold when nonoate was added to the bath at concentrations of 10(-6) to 10(-4) mol/L. 11,12-EET (10(-8) to 10(-4) mol/L) also increased the activity of the K-Ca channels in a concentration-dependent manner, but it had no effect on the activity of the K-drf channels, even in the highest concentration studied (10(-4) mol/L). In contrast to the effect of 11,12-EET, iloprost, a prostaglandin I-2 analogue (10(-6) to 10(-4) mol/L), produced a concentration-dependent increase in the activity of K-drf channels without affecting the K-Ca channels. In conclusion, all three endothelium-derived vasodilators act to open potassium channels; however, the channel types that they affect are different. NO activates both K-Ca and K-drf channels; 11,12-EET activates only the K-Ca channels; and prostaglandin It activates only the K-drf channels.
引用
收藏
页码:262 / 267
页数:6
相关论文
共 35 条
[1]  
ADEAGBO AS, 1989, J PHARMACOL EXP THER, V252, P26
[2]  
ARGUS JR, 1989, PHARMACOL THERAPEUT, V41, P303
[3]   NITRIC-OXIDE DIRECTLY ACTIVATES CALCIUM-DEPENDENT POTASSIUM CHANNELS IN VASCULAR SMOOTH-MUSCLE [J].
BOLOTINA, VM ;
NAJIBI, S ;
PALACINO, JJ ;
PAGANO, PJ ;
COHEN, RA .
NATURE, 1994, 368 (6474) :850-853
[4]   MEMBRANE HYPERPOLARIZATION IS A MECHANISM OF ENDOTHELIUM-DEPENDENT CEREBRAL VASODILATION [J].
BRAYDEN, JE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (03) :H668-H673
[5]   Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors [J].
Campbell, WB ;
Gebremedhin, D ;
Pratt, PF ;
Harder, DR .
CIRCULATION RESEARCH, 1996, 78 (03) :415-423
[6]   HYPERPOLARIZATION OF ARTERIAL SMOOTH-MUSCLE INDUCED BY ENDOTHELIAL HUMORAL SUBSTANCES [J].
CHEN, G ;
YAMAMOTO, Y ;
MIWA, K ;
SUZUKI, H .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (06) :H1888-H1892
[7]  
FALCK JR, 1987, J LIPID RES, V28, P840
[8]   EVIDENCE THAT NITRIC-OXIDE DOES NOT MEDIATE THE HYPERPOLARIZATION AND RELAXATION TO ACETYLCHOLINE IN THE RAT SMALL MESENTERIC-ARTERY [J].
GARLAND, CJ ;
MCPHERSON, GA .
BRITISH JOURNAL OF PHARMACOLOGY, 1992, 105 (02) :429-435
[9]   MECHANISM OF ACTION OF CEREBRAL EPOXYEICOSATRIENOIC ACIDS ON CEREBRAL ARTERIAL SMOOTH-MUSCLE [J].
GEBREMEDHIN, D ;
MA, YH ;
FALCK, JR ;
ROMAN, RJ ;
VANROLLINS, M ;
HARDER, DR .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (02) :H519-H525
[10]   RETRACTED: [CA2+](I) INHIBITION OF K+ CHANNELS IN CANINE RENAL-ARTERY - NOVEL MECHANISM FOR AGONIST-INDUCED MEMBRANE DEPOLARIZATION (Retracted Article. See vol. 94, pg E15, 2004) [J].
GELBAND, CH ;
HUME, JR .
CIRCULATION RESEARCH, 1995, 77 (01) :121-130