Modulation of voltage-dependent K + channel by redox potential in pulmonary and ear arterial smooth muscle cells of the rabbit

1997 ◽  
Vol 434 (6) ◽  
pp. 764-771 ◽  
Author(s):  
M. K. Park ◽  
Young Min Bae ◽  
S. H. Lee ◽  
Won-Kyung Ho ◽  
Y. E. Earm
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Redox Potential ◽  
Muscle Cells ◽  
K Channel ◽  
Arterial Smooth Muscle ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

Inhibition by Imipramine of the Voltage-Dependent K+ Channel in Rabbit Coronary Arterial Smooth Muscle Cells

2020 ◽  
Vol 178 (2) ◽  
pp. 302-310
Author(s):  
Jin Ryeol An ◽  
Mi Seon Seo ◽  
Hee Seok Jung ◽  
Ryeon Heo ◽  
Minji Kang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Arterial Smooth Muscle ◽  
Closed State ◽  
Kv Channels ◽  
State Dependent ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

Abstract Imipramine, a tricyclic antidepressant, is used in the treatment of depressive disorders. However, the effect of imipramine on vascular ion channels is unclear. Therefore, using a patch-clamp technique we examined the effect of imipramine on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells. Kv channels were inhibited by imipramine in a concentration-dependent manner, with an IC50 value of 5.55 ± 1.24 µM and a Hill coefficient of 0.73 ± 0.1. Application of imipramine shifted the steady-state activation curve in the positive direction, indicating that imipramine-induced inhibition of Kv channels was mediated by influencing the voltage sensors of the channels. The recovery time constants from Kv-channel inactivation were increased in the presence of imipramine. Furthermore, the application of train pulses (of 1 or 2 Hz) progressively augmented the imipramine-induced inhibition of Kv channels, suggesting that the inhibitory effect of imipramine is use (state) dependent. The magnitude of Kv current inhibition by imipramine was similar during the first, second, and third depolarizing pulses. These results indicate that imipramine-induced inhibition of Kv channels mainly occurs in the closed state. The imipramine-mediated inhibition of Kv channels was associated with the Kv1.5 channel, not the Kv2.1 or Kv7 channel. Inhibition of Kv channels by imipramine caused vasoconstriction. From these results, we conclude that imipramine inhibits vascular Kv channels in a concentration- and use (closed-state)-dependent manner by changing their gating properties regardless of its own function.

Inhibition of voltage‐dependent K + channels by iloperidone in coronary arterial smooth muscle cells

2020 ◽  
Vol 40 (9) ◽  
pp. 1297-1305 ◽  
Author(s):  
Jin Ryeol An ◽  
Mi Seon Seo ◽  
Hee Seok Jung ◽  
Minji Kang ◽  
Ryeon Heo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

The effect of PI3 kinase inhibitor LY294002 on voltage-dependent K+ channels in rabbit coronary arterial smooth muscle cells

Life Sciences ◽  
2013 ◽  
Vol 92 (17-19) ◽  
pp. 916-922 ◽  
Author(s):  
Da Hye Hong ◽  
Il-Whan Choi ◽  
Youn Kyoung Son ◽  
Dae-Joong Kim ◽  
Sung Hun Na ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Kinase Inhibitor ◽  
Muscle Cells ◽  
Pi3 Kinase ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Voltage Dependent ◽  
Arterial Smooth Muscle Cells

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca2+ in arterial smooth muscle cells and elicits vasocontraction

2011 ◽  
Vol 300 (6) ◽  
pp. H2016-H2026 ◽  
Author(s):  
Neerupma Silswal ◽  
Nikhil K. Parelkar ◽  
Michael J. Wacker ◽  
Marco Brotto ◽  
Jon Andresen
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ryanodine Receptors ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Arterial Smooth Muscle Cells

Phosphoinositide (3,5)-bisphosphate [PI(3,5)P2] is a newly identified phosphoinositide that modulates intracellular Ca2+ by activating ryanodine receptors (RyRs). Since the contractile state of arterial smooth muscle depends on the concentration of intracellular Ca2+, we hypothesized that by mobilizing sarcoplasmic reticulum (SR) Ca2+ stores PI(3,5)P2 would increase intracellular Ca2+ in arterial smooth muscle cells and cause vasocontraction. Using immunohistochemistry, we found that PI(3,5)P2 was present in the mouse aorta and that exogenously applied PI(3,5)P2 readily entered aortic smooth muscle cells. In isolated aortic smooth muscle cells, exogenous PI(3,5)P2 elevated intracellular Ca2+, and it also contracted aortic rings. Both the rise in intracellular Ca2+ and the contraction caused by PI(3,5)P2 were prevented by antagonizing RyRs, while the majority of the PI(3,5)P2 response was intact after blockade of inositol (1,4,5)-trisphosphate receptors. Depletion of SR Ca2+ stores with thapsigargin or caffeine and/or ryanodine blunted the Ca2+ response and greatly attenuated the contraction elicited by PI(3,5)P2. The removal of extracellular Ca2+ or addition of verapamil to inhibit voltage-dependent Ca2+ channels reduced but did not eliminate the Ca2+ or contractile responses to PI(3,5)P2. We also found that PI(3,5)P2 depolarized aortic smooth muscle cells and that LaCl3 inhibited those aspects of the PI(3,5)P2 response attributable to extracellular Ca2+. Thus, full and sustained aortic contractions to PI(3,5)P2 required the release of SR Ca2+, probably via the activation of RyR, and also extracellular Ca2+ entry via voltage-dependent Ca2+ channels.

The Effect of Midazolam on Outward K+Channel Currents in Rabbit Cerebral Arterial Smooth Muscle Cells

2007 ◽  
Vol 52 (1) ◽  
pp. 67
Author(s):  
Young Chul Shin ◽  
Jae Hang Shim ◽  
Woo Jae Jeon ◽  
Sang Yoon Cho ◽  
Woo Jong Shin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
K Channel ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Channel Currents
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