scholarly journals The involvement of L-type Ca2+ channels in the relaxant effects of the ATP-sensitive K+ channel opener ZD6169 on pig urethral smooth muscle

2001 ◽  
Vol 134 (7) ◽  
pp. 1505-1515 ◽  
Author(s):  
Noriyoshi Teramoto ◽  
Takakazu Yunoki ◽  
Shigeoki Ikawa ◽  
Naruaki Takano ◽  
Kiyoshi Tanaka ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
K Channel ◽  
Channel Opener ◽  
Urethral Smooth Muscle ◽  
K Channel Opener ◽  
Ca2 Channels

Effects of BRL 34915, a putative K channel opener, on transmembrane 45Ca movements in rabbit aortic smooth muscle

1988 ◽  
Vol 155 (3) ◽  
pp. 229-237 ◽  
Author(s):  
Peter J.S. Chiu ◽  
Glen Tetzloff ◽  
Ho-Sam Ahn ◽  
Edmund J. Sybertz
Keyword(s):  
Smooth Muscle ◽  
K Channel ◽  
Aortic Smooth Muscle ◽  
Channel Opener ◽  
K Channel Opener

Venoconstriction to endothelin-1 in humans: role of calcium and potassium channels

1993 ◽  
Vol 265 (5) ◽  
pp. H1676-H1681 ◽  
Author(s):  
W. G. Haynes ◽  
D. J. Webb
Keyword(s):  
Human Subjects ◽  
K Channel ◽  
K Channels ◽  
Endothelin 1 ◽  
Channel Opener ◽  
K Channel Opener ◽  
Ca2 Channels

Recent studies in vitro have suggested that there may be an interaction between endothelin-1 and ATP-sensitive K+ channels in vascular smooth muscle. Here we have investigated whether agents acting on membrane Ca2+ and K+ channels modulate endothelin-1-induced venoconstriction in vivo in human subjects. In a series of studies, six healthy subjects received, on separate occasions, local infusions into dorsal hand veins of endothelin-1 coinfused with 1) the ATP-sensitive K+ channel opener, cromakalim; 2) the dihydropyridine Ca2+ antagonist, nicardipine; 3) a control vasodilator, hydralazine; and 4) saline placebo. Endothelin-1 caused local venoconstriction with a maximum reduction in vein size of 66 +/- 4% at 60 min (P = 0.0001 vs. basal). Cromakalim prevented endothelin-1-induced venoconstriction (9 +/- 10% maximum constriction; P = 0.68 vs. basal). By contrast, nicardipine, in a dose sufficient to block depolarization-induced constriction caused by K+ infusion, had only a partial effect on endothelin-1-induced venoconstriction (35 +/- 8% maximum constriction; P = 0.001 vs. basal; P = 0.02 vs. endothelin-1), whereas a 10-fold higher dose of nicardipine had no additional effect and hydralazine had no effect. In further studies, cromakalim, but not nicardipine, reversed endothelin-1-induced venoconstriction. Cromakalim did not prevent constriction induced by norepinephrine. Although calcium entry through dihydropyridine-sensitive Ca2+ channels may account in part for the vasoconstrictor action of endothelin-1 in humans, the abolition of endothelin-1 responses by a K+ channel opener suggests additional mechanisms of action for endothelin-1.

Electrophysiological actions of a novel K+ channel opener MCC-134 on rabbit portal vein smooth muscle

1999 ◽  
Vol 384 (2-3) ◽  
pp. 203-212 ◽  
Author(s):  
Hiromitsu Morita ◽  
Kazunori Yamada ◽  
Kihachiro Abe ◽  
Yushi Ito ◽  
Ryuji Inoue
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
K Channel ◽  
Channel Opener ◽  
Rabbit Portal Vein ◽  
K Channel Opener
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