Further characterization of the effects of imipramine on plateau membrane currents in guinea-pig ventricular myocytes

1991 ◽  
Vol 344 (6) ◽  
Author(s):  
Eva Delp�n ◽  
Juan Tamargo ◽  
Jos� S�nchez-Chapula
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Membrane Currents

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.

Effects of Tilisolol, a Nonselective β-Adrenergic Blocker, on the Membrane Currents of Isolated Guinea Pig Ventricular Myocytes

1997 ◽  
Vol 29 (5) ◽  
pp. 593-598 ◽  
Author(s):  
Shuichi Takagi ◽  
Yasuki Kihara ◽  
Tamotsu Mitsuiye ◽  
Zhuren Wang ◽  
Shigetake Sasayama
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Adrenergic Blocker

Effects of SN-6, a novel NCX inhibitor on membrane currents in guinea pig cardiac ventricular myocytes

2006 ◽  
Vol 41 (6) ◽  
pp. 1072-1072
Author(s):  
Y WATANABE ◽  
C NIU ◽  
T IWAMOTO ◽  
K YAMASHITA ◽  
H SATOH ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Cardiac Ventricular Myocytes

Ca2+ current and Ca2+ transients under action potential clamp in guinea pig ventricular myocytes

1991 ◽  
Vol 261 (2) ◽  
pp. C393-C397 ◽  
Author(s):  
J. Arreola ◽  
R. T. Dirksen ◽  
R. C. Shieh ◽  
D. J. Williford ◽  
S. S. Sheu
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Slow Component ◽  
Fast Component ◽  
Maximal Effect ◽  
The Relationship ◽  
Peak Value

Precise characterization of the magnitude and kinetics of transsarcolemmal Ca2+ influx during an action potential (AP) is essential for a complete understanding of excitation-contraction coupling in heart. Using a voltage-clamp protocol that simulated a physiological AP (AP clamp), we characterized the properties of the Ca2+ current (ICa) in guinea pig ventricular myocytes. The AP-generated ICa showed a complex time course that was different from ICa generated by a square pulse. ICa activated rapidly during the upstroke of the AP and then partially inactivated during the plateau. The fast component of ICa reached a peak value of -7.6 +/- 1.0 pA/pF at 2.40 +/- 0.30 ms after depolarization, followed by a slow component with a peak value of -2.9 +/- 0.4 pA/pF during the plateau. ICa generated by an AP was composed of both L- and T-type Ca2+ channels. T-type Ca2+ current contributed to the fast component of ICa and L-type Ca2+ current contributed to both fast and slow components of ICa. Activation of beta-adrenoceptors enhanced ICa with a maximal effect lasting throughout the entire plateau of the AP. Measurements of cytosolic Ca2+ transients using fura-2 indicated that the ICa was responsible for triggering Ca2+ release from the sarcoplasmic reticulum. The AP clamp provides a new approach for investigation of the relationship between ICa and Ca2+ transients under more physiological conditions.

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