Simultaneous recording of ATP-sensitive K+ current and intracellular Ca2+ in anoxic rat ventricular myocytes. Effects of glibenclamide

1996 ◽  
Vol 432 (1) ◽  
pp. 75-80 ◽  
Author(s):  
U. Ruß ◽  
H. Englert ◽  
B. A. Schölkens ◽  
H. Gögelein
2001 ◽  
Vol 537 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Jean‐Pierre Bénitah ◽  
Emeline Perrier ◽  
Ana María Gómez ◽  
Guy Vassort

2000 ◽  
Vol 52 (1) ◽  
pp. 99-105 ◽  
Author(s):  
MICHIKO HIROTA ◽  
HISAKAZU OHTANI ◽  
ERIKA HANADA ◽  
HITOSHI SATO ◽  
HAJIME KOTAKI ◽  
...  

1989 ◽  
Vol 257 (5) ◽  
pp. H1746-H1749 ◽  
Author(s):  
I. D. Dukes ◽  
M. Morad

The action of tedisamil, a new bradycardiac agent with antiarrhythmic properties, was investigated in single rat ventricular myocytes using the whole cell voltage-clamp technique. Under current clamp conditions, 1-20 microM tedisamil caused marked prolongations of the action potential. Over the same concentration range, in voltage-clamped myocytes, tedisamil suppressed the transient outward current (ito) and enhanced its inactivation in a dose-dependent manner. The half-maximal dose for the effect of tedisamil on ito was approximately 6 microM. Tedisamil had no significant effects on the inwardly rectifying potassium current and calcium current but did suppress the sodium current at concentrations greater than 20 microM. Our findings suggest that tedisamil represents a new type of antiarrhythmic agent that primarily suppresses the transient outward K+ current.


Circulation ◽  
2012 ◽  
Vol 126 (24) ◽  
pp. 2809-2818 ◽  
Author(s):  
Sadguna Y. Balijepalli ◽  
Evi Lim ◽  
Sarah P. Concannon ◽  
Chen L. Chew ◽  
Kassandra E. Holzem ◽  
...  

1997 ◽  
Vol 272 (4) ◽  
pp. H1741-H1750 ◽  
Author(s):  
L. H. Xie ◽  
M. Takano ◽  
A. Noma

The ATP-sensitive K+ current (I(K,ATP)), the inward rectifier K+ current (I(K1)), and the acetylcholine-activated K+ current (I(K,ACh)) were recorded in fetal, neonatal, and adult rat ventricular myocytes using the patch-clamp technique. The density (pA/pF) of I(K1) increased from gestation day 10 through neonatal day 1 and then decreased after neonatal day 30. The density of I(K,ATP) activated maximally by metabolic inhibition changed in parallel with the I(K1) density, and the density of I(K,ATP) channel distribution was 1.3 times higher than that of I(K1) throughout the development. We failed to observe developmental changes in the single-channel conductance and the mean open time of I(K1) and I(K,ATP) channels. However, the open probability of the I(K,ATP) channel was lower in fetuses, and the sensitivity to ATP was highest in 1-day neonates. I(K,ACh) were present in the ventricle at all stages of development but at a much lower density than in atrium. The relationship between the resting membrane potential and the development of the inwardly rectifying K-channel family is discussed.


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