scholarly journals The ionic basis of concentration-related effects of noradrenaline on the action potential of calf cardiac purkinje fibres.

1982 ◽  
Vol 322 (1) ◽  
pp. 541-558 ◽  
Author(s):  
R S Kass ◽  
S E Wiegers
Keyword(s):  
Action Potential ◽  
Purkinje Fibres ◽  
Cardiac Purkinje Fibres ◽  
Ionic Basis

Effects of seven drugs of abuse on action potential repolarisation in sheep cardiac Purkinje fibres

2005 ◽  
Vol 511 (2-3) ◽  
pp. 99-107 ◽  
Author(s):  
Robert D. Sheridan ◽  
Simon R. Turner ◽  
Graham J. Cooper ◽  
John E.H. Tattersall
Keyword(s):  
Action Potential ◽  
Drugs Of Abuse ◽  
Purkinje Fibres ◽  
Cardiac Purkinje Fibres

Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Patch Clamp Technique ◽  
17Β Estradiol ◽  
Electrophysiological Effects ◽  
Ionic Basis

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.

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