Role of intracellular calcium in the transient outward current of calf Purkinje fibres

Nature ◽  
1977 ◽  
Vol 269 (5629) ◽  
pp. 611-613 ◽  
Author(s):  
S. A. SIEGELBAUM ◽  
R. W. TSIEN ◽  
R. S. KASS
2010 ◽  
Vol 21 (6) ◽  
pp. 697-703 ◽  
Author(s):  
MIN DONG ◽  
SUJUAN YAN ◽  
YAMEI CHEN ◽  
PAUL J. NIKLEWSKI ◽  
XIAOYIN SUN ◽  
...  

2010 ◽  
Vol 98 (3) ◽  
pp. 360a-361a
Author(s):  
Min Dong ◽  
Sujuan Yan ◽  
Paul Niklewski ◽  
Yamei Chen ◽  
Hong-Sheng Wang

2007 ◽  
Vol 293 (4) ◽  
pp. H2168-H2177 ◽  
Author(s):  
Scott A. Grandy ◽  
Véronique Trépanier-Boulay ◽  
Céline Fiset

To better understand the mechanisms that underlie cardiac repolarization abnormalities in the immature heart, this study characterized and compared K+ currents in mouse ventricular myocytes from day 1, day 7, day 20, and adult CD1 mice to determine the effects of postnatal development on ventricular repolarization. Current- and patch-clamp techniques were used to examine action potentials and the K+ currents underlying repolarization in isolated myocytes. RT-PCR was used to quantify mRNA expression for the K+ channels of interest. This study found that action potential duration (APD) decreased as age increased, with the shortest APDs observed in adult myocytes. This study also showed that K+ currents and the mRNA relative abundance for the various K+ channels were significantly greater in adult myocytes compared with day 1 myocytes. Examination of the individual components of total K+ current revealed that the inward rectifier K+ current ( IK1) developed by day 7, both the Ca2+-independent transient outward current ( Ito) and the steady-state outward K+ current ( Iss) developed by day 20, and the ultrarapid delayed rectifier K+ current ( IKur) did not fully develop until the mouse reached maturity. Interestingly, the increase in IKur was not associated with a decrease in APD. Comparison of atrial and ventricular K+ currents showed that Ito and IKur density were significantly greater in day 7, day 20, and adult myocytes compared with age-matched atrial cells. Overall, it appears that, in mouse ventricle, developmental changes in APD are likely attributable to increases in Ito, Iss, and IK1, whereas the role of IKur during postnatal development appears to be less critical to APD.


1991 ◽  
Vol 260 (5) ◽  
pp. H1501-H1506 ◽  
Author(s):  
Z. G. Wang ◽  
B. Fermini ◽  
S. Nattel

It has long been known that ventricular epicardial action potential duration (APD) is shorter than endocardial, and recent evidence suggests that a larger transient outward current (Ito) in epicardium is responsible for the difference. To evaluate possible corresponding regional variations in atrial tissue, we studied guinea pig atrial epicardial and endocardial action potentials using standard microelectrode techniques. Epicardial APD was consistently shorter than endocardial, but the difference was greatly diminished by rapid pacing or early premature activation, situations in which Ito availability should be limited. 4-Aminopyridine (4-AP), at concentrations (0.5 mM) producing specific Ito blockade, increased APD significantly in atrial epicardium without affecting endocardium. The effect of 4-AP on APD was most marked at slow rates, at which Ito would be greatest, and was negligible at rapid rates or during premature activation, during which Ito would be largely inactivated. At larger concentrations (5 mM) 4-AP caused an equalization of epicardial and endocardial APD. The equimolar substitution of strontium for calcium did not affect APD at slow rates and increased APD (particularly in endocardium) at rapid rates, suggesting that the Ito underlying endocardial-epicardial differences was unlikely to be calcium dependent. We conclude that epicardial-endocardial differences in APD, well documented in ventricular tissue, can also occur in atrial tissue and that the underlying ionic mechanisms appear to be similar.


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