31 research outputs found
From Action Potential-Clamp to "Onion-Peeling" Technique – Recording of Ionic Currents Under Physiological Conditions
Profile of L-Type Ca2+ Current and Na+/Ca2+ Exchange Current during Cardiac Action Potential in Ventricular Myocytes
Beta-adrenergic stimulation reverses the I Kr-I Ks dominant pattern during cardiac action potential.
CaMKII Regulation of the Dynamic L-Type Ca2+ Current and Na+/Ca2+ Exchange Current During Action Potential in Cardiac Myocytes
Cesium increases intracellular uptake of 45 CA 2+ and increases force development in cardiac ventricular muscle during the evolution of early after-depolarizations
Sarcomere Shortening Destabilizes the Ca2+ Control System in Ventricular Myocytes: Implications for Understanding Arrhythmias in Familial Hypertrophic Cardiomyopathy
15+ MILLION TOP 1% MOST CITED SCIENTIST 12.2% AUTHORS AND EDITORS FROM TOP 500 UNIVERSITIES 7 From Action Potential-Clamp to "Onion-Peeling" Technique -Recording of Ionic Currents Under Physiological Conditions
Role of Gap Junction Channel in the Development of Beat-to-Beat Action Potential Repolarization Variability and Arrhythmias
Beta-adrenergic stimulation reverses the IKr–IKs dominant pattern during cardiac action potential
β-Adrenergic stimulation differentially modulates different K(+) channels and thus fine-tunes cardiac action potential (AP) repolarization. However, it remains unclear how the proportion of I Ks, I Kr, and I K1 currents in the same cell would be altered by β-adrenergic stimulation, which would change the relative contribution of individual K(+) current to the total repolarization reserve. In this study, we used an innovative AP-clamp sequential dissection technique to directly record the dynamic I Ks, I Kr, and I K1 currents during the AP in guinea pig ventricular myocytes under physiologically relevant conditions. Our data provide quantitative measures of the magnitude and time course of I Ks, I Kr, and I K1 currents in the same cell under its own steady-state AP, in a physiological milieu, and with preserved Ca(2+) homeostasis. We found that isoproterenol treatment significantly enhanced I Ks, moderately increased I K1, but slightly decreased I Kr in a dose-dependent manner. The dominance pattern of the K(+) currents was I Kr > I K1 > I Ks at the control condition, but reversed to I Kr < I K1 < I Ks following β-adrenergic stimulation. We systematically determined the changes in the relative contribution of I Ks, I Kr, and I K1 to cardiac repolarization during AP at different adrenergic states. In conclusion, the β-adrenergic stimulation fine-tunes the cardiac AP morphology by shifting the power of different K(+) currents in a dose-dependent manner. This knowledge is important for designing antiarrhythmic drug strategies to treat hearts exposed to various sympathetic tones