PCR-based analysis of voltage-gated K+ channels in vascular smooth muscle

1995 ◽  
Vol 145 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Peter Zahradka ◽  
Karen D. Harris ◽  
Barbara Triggs-Raine ◽  
Ginette Lamontagne ◽  
Normand Leblanc
2010 ◽  
Vol 103 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Eun A. Ko ◽  
Won Sun Park ◽  
Amy L. Firth ◽  
Nari Kim ◽  
Jason X.-J. Yuan ◽  
...  

2001 ◽  
Vol 89 (11) ◽  
pp. 1030-1037 ◽  
Author(s):  
Kevin S. Thorneloe ◽  
Tim T. Chen ◽  
Paul M. Kerr ◽  
Elizabeth F. Grier ◽  
Burton Horowitz ◽  
...  

2003 ◽  
Vol 99 (3) ◽  
pp. 666-677 ◽  
Author(s):  
Takashi Akata ◽  
Tomoo Kanna ◽  
Jun Yoshino ◽  
Shosuke Takahashi

Background Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries. Methods Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the beta-escin membrane-permeabilized strips. Results Isoflurane (3-5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 microM) or KCl (40 mM). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl- channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the beta-escin-permeabilized strips. Conclusions In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl- channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.


1999 ◽  
Vol 382 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Sabine Seitz ◽  
Jörg W Wegener ◽  
Johanna Rupp ◽  
Makino Watanabe ◽  
Andreas Jost ◽  
...  

2021 ◽  
Vol 891 ◽  
pp. 173707
Author(s):  
Mi Seon Seo ◽  
Jin Ryeol An ◽  
Hee Seok Jung ◽  
Minji Kang ◽  
Ryeon Heo ◽  
...  

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