Effects of extracellular potassium ions on outward potassium current dependent on extracellular calcium ions

1988 ◽  
Vol 19 (3) ◽  
pp. 260-264
Author(s):  
A. E. Martynyuk
Keyword(s):  
Calcium Ions ◽  
Potassium Current ◽  
Extracellular Calcium ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Outward Potassium Current

scholarly journals A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome

2008 ◽  
Vol 81 (4) ◽  
pp. 686-694 ◽  
Author(s):  
K. Calloe ◽  
J. M. Cordeiro ◽  
J. M. Di Diego ◽  
R. S. Hansen ◽  
M. Grunnet ◽  
...  
Keyword(s):  
Brugada Syndrome ◽  
Potassium Current ◽  
Transient Outward Potassium Current ◽  
Outward Potassium Current

Nitrendipine blocks high potassium contractures but not twitches in rat skeletal muscle

1988 ◽  
Vol 66 (9) ◽  
pp. 1210-1213 ◽  
Author(s):  
G. B. Frank ◽  
L. Konya ◽  
T. Subrahmanyam Sudha
Keyword(s):  
Skeletal Muscle ◽  
Calcium Ions ◽  
Calcium Uptake ◽  
Channel Blocker ◽  
Mechanical Response ◽  
Extracellular Calcium ◽  
The Other ◽  
Rat Skeletal Muscle ◽  
Potassium Depolarization ◽  
High Potassium

The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10−7 to 5 × 10−5 M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-senstitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation–contraction (E–C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E–C coupling during the twitch.

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