Quinidine inhibition of the muscarine receptor-activated K+ channel current in atrial cells of guinea pig

1987 ◽  
Vol 335 (2) ◽  
Author(s):  
Yoshihisa Kurachi ◽  
Toshiaki Nakajima ◽  
Tsuneaki Sugimoto
Keyword(s):  
Guinea Pig ◽  
K Channel ◽  
Muscarine Receptor ◽  
Channel Current ◽  
Atrial Cells

Inhibitory effects of class I and IV antiarrhythmic drugs on the Na+-activated K+ channel current in guinea pig ventricular cells

1998 ◽  
Vol 358 (6) ◽  
pp. 641-648 ◽  
Author(s):  
Katsumi Mori ◽  
Satoru Kobayashi ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
H. Nakaya
Keyword(s):  
Guinea Pig ◽  
Antiarrhythmic Drugs ◽  
Class I ◽  
K Channel ◽  
Inhibitory Effects ◽  
Channel Current ◽  
Ventricular Cells

scholarly journals Glibenclamide Specifically Blocks ATP-Sensitive K<+ Channel Current in Atrial Myocytes of Guinea Pig Heart

1990 ◽  
Vol 54 (4) ◽  
pp. 473-477 ◽  
Author(s):  
Eiji HAMADA ◽  
Reiko TAKIKAWA ◽  
Hiroyuki ITO ◽  
Mari IGUCHI ◽  
Akira TERANO ◽  
...  
Keyword(s):  
Guinea Pig ◽  
K Channel ◽  
Atrial Myocytes ◽  
Guinea Pig Heart ◽  
Channel Current

Acetylcholine-mediated K+ channel activity in guinea-pig atrial cells is supported by nucleoside diphosphate kinase

1993 ◽  
Vol 422 (4) ◽  
pp. 316-324 ◽  
Author(s):  
Hein Heidb�chel ◽  
Geert Callewaert ◽  
Johan Vereecke ◽  
Edward Carmeliet
Keyword(s):  
Guinea Pig ◽  
Nucleoside Diphosphate Kinase ◽  
K Channel ◽  
Channel Activity ◽  
Atrial Cells

Coenzyme Q10 attenuates cyanide-activation of the ATP-sensitive K+ channel current in single cardiac myocytes of the guinea-pig

1991 ◽  
Vol 344 (1) ◽  
Author(s):  
Hiroyuki Ito ◽  
Toshiaki Nakajima ◽  
Reiko Takikawa ◽  
Eiji Hamada ◽  
Mari Iguchi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Coenzyme Q10 ◽  
K Channel ◽  
Channel Current

scholarly journals Large-conductance voltage- and Ca2+-activated K+ channel regulation by protein kinase C in guinea pig urinary bladder smooth muscle

2014 ◽  
Vol 306 (5) ◽  
pp. C460-C470 ◽  
Author(s):  
Kiril L. Hristov ◽  
Amy C. Smith ◽  
Shankar P. Parajuli ◽  
John Malysz ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Bk Channels ◽  
Bk Channel ◽  
K Channel ◽  
Channel Activity ◽  
Open Probability ◽  
Channel Regulation ◽  
Pkc Activation

Large-conductance voltage- and Ca2+-activated K+ (BK) channels are critical regulators of detrusor smooth muscle (DSM) excitability and contractility. PKC modulates the contraction of DSM and BK channel activity in non-DSM cells; however, the cellular mechanism regulating the PKC-BK channel interaction in DSM remains unknown. We provide a novel mechanistic insight into BK channel regulation by PKC in DSM. We used patch-clamp electrophysiology, live-cell Ca2+ imaging, and functional studies of DSM contractility to elucidate BK channel regulation by PKC at cellular and tissue levels. Voltage-clamp experiments showed that pharmacological activation of PKC with PMA inhibited the spontaneous transient BK currents in native freshly isolated guinea pig DSM cells. Current-clamp recordings revealed that PMA significantly depolarized DSM membrane potential and inhibited the spontaneous transient hyperpolarizations in DSM cells. The PMA inhibitory effects on DSM membrane potential were completely abolished by the selective BK channel inhibitor paxilline. Activation of PKC with PMA did not affect the amplitude of the voltage-step-induced whole cell steady-state BK current or the single BK channel open probability (recorded in cell-attached mode) upon inhibition of all major Ca2+ sources for BK channel activation with thapsigargin, ryanodine, and nifedipine. PKC activation with PMA elevated intracellular Ca2+ levels in DSM cells and increased spontaneous phasic and nerve-evoked contractions of DSM isolated strips. Our results support the concept that PKC activation leads to a reduction of BK channel activity in DSM via a Ca2+-dependent mechanism, thus increasing DSM contractility.

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