scholarly journals A Carbohydrate Fraction, AIP1, fromArtemisia IwayomogiReduces the Action Potential Duration by Activation of Rapidly Activating Delayed Rectifier K+Channels in Rabbit Ventricular Myocytes

2010 ◽  
Vol 14 (3) ◽  
pp. 119 ◽  
Author(s):  
Won Sun Park ◽  
Youn Kyoung Son ◽  
Eun A Ko ◽  
Seong Woo Choi ◽  
Nari Kim ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Delayed Rectifier ◽  
K Channels ◽  
Carbohydrate Fraction ◽  
Rabbit Ventricular Myocytes

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
Gui-Rong Li ◽  
Min Zhang ◽  
Leslie S. Satin ◽  
Clive M. Baumgarten
Keyword(s):  
Action Potential ◽  
Cell Volume ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Current Clamp ◽  
Osmotic Swelling ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Fura 2 ◽  
Rabbit Ventricular Myocytes

We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current ( I Ca-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given I Ca-L, and later, both I Ca-L and the Ca2+ transient are inhibited.

L-364,373 (R-L3) enantiomers have opposite modulating effects on IKs in mammalian ventricular myocytes

2013 ◽  
Vol 91 (8) ◽  
pp. 586-592 ◽  
Author(s):  
Claudia Corici ◽  
Zsófia Kohajda ◽  
Attila Kristóf ◽  
András Horváth ◽  
László Virág ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Guinea Pig ◽  
Action Potential ◽  
Right Ventricular ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Ventricular Arrhythmias ◽  
Ventricular Myocytes ◽  
Delayed Rectifier ◽  
Whole Cell Patch Clamp

Activators of the slow delayed rectifier K+ current (IKs) have been suggested as promising tools for suppressing ventricular arrhythmias due to prolongation of repolarization. Recently, L-364,373 (R-L3) was nominated to activate IKs in myocytes from several species; however, in some studies, it failed to activate IKs. One later study suggested opposite modulating effects from the R-L3 enantiomers as a possible explanation for this discrepancy. Therefore, we analyzed the effect of the RL-3 enantiomers on IKs in ventricular mammalian myocytes, by applying standard microelectrode and whole-cell patch-clamp techniques at 37 °C. We synthesized 2 substances, ZS_1270B (right) and ZS_1271B (left), the 2 enantiomers of R-L3. In rabbit myocytes, ZS_1270B enhanced the IKs tail current by approximately 30%, whereas ZS_1271B reduced IKs tails by 45%. In guinea pig right ventricular preparations, ZS_1270B shortened APD90 (action potential duration measured at 90% repolarization) by 12%, whereas ZS_1271B lengthened it by approximately 15%. We concluded that R-L3 enantiomers in the same concentration range indeed have opposite modulating effects on IKs, which may explain why the racemic drug R-L3 previously failed to activate IKs. ZS_1270B is a potent IKs activator, therefore, this substance is appropriate to test whether IKs activators are ideal tools to suppress ventricular arrhythmias originating from prolongation of action potentials.

scholarly journals Action Potential Duration Restitution and Alternans in Rabbit Ventricular Myocytes

2005 ◽  
Vol 96 (4) ◽  
pp. 459-466 ◽  
Author(s):  
Joshua I. Goldhaber ◽  
Lai-Hua Xie ◽  
Tan Duong ◽  
Christi Motter ◽  
Kien Khuu ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Rabbit Ventricular Myocytes ◽  
Action Potential Duration Restitution

Altered K+ current profiles underlie cardiac action potential shortening in hyperkalemia and β-adrenergic stimulation

2019 ◽  
Vol 97 (8) ◽  
pp. 773-780 ◽  
Author(s):  
Bence Hegyi ◽  
Ye Chen-Izu ◽  
Leighton T. Izu ◽  
Tamás Bányász
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Delayed Rectifier ◽  
Adrenergic Stimulation ◽  
Compensatory Mechanisms ◽  
Phase 3 ◽  
K Current ◽  
Rabbit Ventricular Myocytes ◽  
Action Potential Shortening ◽  
Stimulation Of

Hyperkalemia is known to develop in various conditions including vigorous physical exercise. In the heart, hyperkalemia is associated with action potential (AP) shortening that was attributed to altered gating of K+ channels. However, it remains unknown how hyperkalemia changes the profiles of each K+ current under a cardiac AP. Therefore, we recorded the major K+ currents (inward rectifier K+ current, IK1; rapid and slow delayed rectifier K+ currents, IKr and IKs, respectively) using AP-clamp in rabbit ventricular myocytes. As K+ may accumulate at rapid heart rates during sympathetic stimulation, we also examined the effect of isoproterenol on these K+ currents. We found that IK1 was significantly increased in hyperkalemia, whereas the reduction of driving force for K+ efflux dominated over the altered channel gating in case of IKr and IKs. Overall, the markedly increased IK1 in hyperkalemia overcame the relative decreases of IKr and IKs during AP, resulting in an increased net repolarizing current during AP phase 3. β-Adrenergic stimulation of IKs also provided further repolarizing power during sympathetic activation, although hyperkalemia limited IKs upregulation. These results indicate that facilitation of IK1 in hyperkalemia and β-adrenergic stimulation of IKs represent important compensatory mechanisms against AP prolongation and arrhythmia susceptibility.

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