Action Potential Prolongation and Potassium Currents in Left-Ventricular Myocytes Isolated from Hypertrophied Rabbit Hearts

1998 ◽  
Vol 30 (1) ◽  
pp. 43-53 ◽  
Author(s):  
MA McIntosh ◽  
SM Cobbe ◽  
KA Kane ◽  
AC Rankin
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Potassium Currents ◽  
Left Ventricular ◽  
Action Potential Prolongation

scholarly journals The effect of swimming exercise on age-dependent electrophysiological changes in female rat myocardium

2020 ◽  
Vol 72 (3) ◽  
pp. 393-401
Author(s):  
Nihal Ozturk ◽  
Semir Ozdemir
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Potassium Currents ◽  
The Elderly ◽  
Left Ventricular ◽  
Female Rats ◽  
Swimming Exercise ◽  
Female Rat ◽  
Rat Hearts ◽  
Age Dependent

The effects of swimming exercise on age-associated electrical changes in female rat hearts were investigated. Four- and 24-month-old Wistar female rats were divided into three groups as follows: sedentary young, sedentary old and exercise old. Swimming exercise was performed for 8 weeks (60 min/day, 5 days/week). All recordings were taken from freshly isolated left ventricular myocytes of rat heart. Aging caused a significant increase in the size of myocytes; swimming exercise did not affect this change. The repolarization period of the action potential was prolonged in aged myocytes, but exercise training had no effect on this prolongation. Exercise suppressed the transient outward potassium currents, while the inactivation and reactivation kinetics did not change between the groups. Moreover, aging caused suppression in the inward rectifier potassium currents, and exercise increased this suppression. Consequently, changes in the action potential and potassium currents may contribute to the impaired cardiac function in the elderly female myocardium, and swimming exercise is not an effective strategy in reversing these electrical changes.

Modeling of IK1 mutations in human left ventricular myocytes and tissue

2007 ◽  
Vol 292 (1) ◽  
pp. H549-H559 ◽  
Author(s):  
Gunnar Seemann ◽  
Frank B. Sachse ◽  
Daniel L. Weiss ◽  
Louis J. Ptáček ◽  
Martin Tristani-Firouzi
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Ventricular Myocytes ◽  
Torsade De Pointes ◽  
Low Frequency ◽  
Mechanistic Explanation ◽  
Left Ventricular ◽  
Autosomal Dominant Disorder ◽  
Modeling Approach ◽  
Dispersion Of Repolarization

Elucidation of the cellular basis of arrhythmias in ion channelopathy disorders is complicated by the inherent difficulties in studying human cardiac tissue. Thus we used a computer modeling approach to study the mechanisms of cellular dysfunction induced by mutations in inward rectifier potassium channel (Kir)2.1 that cause Andersen-Tawil syndrome (ATS). ATS is an autosomal dominant disorder associated with ventricular arrhythmias that uncommonly degenerate into the lethal arrhythmia torsade de pointes. We simulated the cellular and tissue effects of a potent disease-causing mutation D71V Kir2.1 with mathematical models of human ventricular myocytes and a bidomain model of transmural conduction. The D71V Kir2.1 mutation caused significant action potential duration prolongation in subendocardial, midmyocardial, and subepicardial myocytes but did not significantly increase transmural dispersion of repolarization. Simulations of the D71V mutation at shorter cycle lengths induced stable action potential alternans in midmyocardial, but not subendocardial or subepicardial cells. The action potential alternans was manifested as an abbreviated QRS complex in the transmural ECG, the result of action potential propagation failure in the midmyocardial tissue. In addition, our simulations of D71V mutation recapitulate several key ECG features of ATS, including QT prolongation, T-wave flattening, and QRS widening. Thus our modeling approach faithfully recapitulates several features of ATS and provides a mechanistic explanation for the low frequency of torsade de pointes arrhythmia in ATS.

Increasing DHA and EPA Concentrations Prolong Action Potential Durations and Reduce Transient Outward Potassium Currents in Rat Ventricular Myocytes

Lipids ◽  
2010 ◽  
Vol 46 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Hong-Xia Li ◽  
Ru-Xing Wang ◽  
Xiao-Rong Li ◽  
Tao Guo ◽  
Ying Wu ◽  
...  
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Potassium Currents ◽  
Rat Ventricular Myocytes

Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development

2007 ◽  
Vol 293 (6) ◽  
pp. H3301-H3310 ◽  
Author(s):  
Ye Chen-Izu ◽  
Ling Chen ◽  
Tamás Bányász ◽  
Stacey L. McCulle ◽  
Byron Norton ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Heart Disease ◽  
Action Potential ◽  
Cardiac Hypertrophy ◽  
Ventricular Myocytes ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Window Period ◽  
Coupling System

Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling. However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic Ca2+ transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the Ca2+ transient. Functionally, augmented Ca2+ transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased Ca2+ signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed.

Transient Receptor Potential Vanilloid 4 channel participates in mouse ventricular electrical activity

2021 ◽  
Author(s):  
Sebastien Chaigne ◽  
Guillaume Cardouat ◽  
Julien Louradour ◽  
Fanny Vaillant ◽  
Sabine Charron ◽  
...  
Keyword(s):  
Action Potential ◽  
Electrical Activity ◽  
Transient Receptor Potential ◽  
Ventricular Myocytes ◽  
Receptor Potential ◽  
Left Ventricular ◽  
Transient Receptor Potential Vanilloid ◽  
Western Blots ◽  
Transient Receptor ◽  
Trpv4 Channel

Introduction: Transient Receptor Potential Vanilloid 4 (TRPV4) channel is a calcium permeable channel (PCa/PNa ~ 10). Its expression was reported in ventricular myocytes where it is involved in several cardiac pathological mechanisms. In this study, we investigated the implication of TRPV4 in ventricular electrical activity. Methods and Results: Left ventricular myocytes were isolated from trpv4+/+ and trpv4-/- mice. TRPV4 membrane expression and its colocalization with Cav1.2 was confirmed using western-blots biotinylation, immunoprecipitation and immunostaining experiments. Then, electrocardiograms (ECGs) and patch-clamp recordings showed shortened QTc and action potential (AP) duration in trpv4-/- compared to trpv4+/+ mice. Thus, TRPV4 activator GSK1016790A produced a transient and dose-dependent increase in AP duration at 90 % of repolarization (APD90) in trpv4+/+, but not in trpv4-/- myocytes or when combined with TRPV4 inhibitor GSK2193874 (100 nM). Hence, GSK1016790A increased CaT amplitude in trpv4+/+ but not in trpv4-/- myocytes, suggesting that TRPV4 carries an inward Ca2+ current in myocytes. Conversely, TRPV4 inhibitor GSK2193874 (100 nM) alone reduced APD90 in trpv4+/+ but not in trpv4-/- myocytes, suggesting that TRPV4 prolongs AP duration (APD) in basal condition. Finally, introducing TRPV4 parameters in a mathematical model predicted the development of an inward TRPV4 current during repolarization that increases AP duration and CaT amplitude, in accordance with what found experimentally. Conclusion: This study shows for the first time that TRPV4 modulates AP and QTc durations and constitutes thereby a good therapeutical target against long QT-mediated ventricular arrhythmias. Keywords: TRPV4 channel, action potential, QT interval, mathematical modeling, trpv4-/-, calcium transient.

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