Transmembrane ICa contributes to rate-dependent changes of action potentials in human ventricular myocytes Export

@article{citeulike:1533174, abstract = {The mechanism of action potential abbreviation caused by increasing rate in human ventricular myocytes is unknown. The present study was designed to determine the potential role of Ca2+ current (ICa) in the rate-dependent changes in action potential duration (APD) in human ventricular cells. Myocytes isolated from the right ventricle of explanted human hearts were studied at 36{degrees}C with whole cell voltage and current-clamp techniques. APD at 90\% repolarization decreased by 36 {+/-} 4\% when frequency increased from 0.5 to 2 Hz. Equimolar substitution of Mg2+ for Ca2+ significantly decreased rate-dependent changes in APD (to 6 {+/-} 3\%, P < 0.01). Peak ICa was decreased by 34 {+/-} 3\% from 0.5 to 2 Hz (P < 0.01), and ICa had recovery time constants of 65 {+/-} 12 and 683 {+/-} 39 ms at [-]80 mV. Action potential clamp demonstrated a decreasing contribution of ICa during the action potential as rate increased. The rate-dependent slow component of the delayed rectifier K+ current (IKs) was not observed in four cells with an increase in frequency from 0.5 to 3.3 Hz, perhaps because the IKs is so small that the increase at a high rate could not be seen. These results suggest that reduction of Ca2+ influx during the action potential accounts for most of the rate-dependent abbreviation of human ventricular APD.}, author = {Li, Gui-Rong and Yang, Baofeng and Feng, Jianlin and Bosch, Ralph F. and Carrier, Michel and Nattel, Stanley}, citeulike-article-id = {1533174}, citeulike-linkout-0 = {http://ajpheart.physiology.org/cgi/content/abstract/276/1/H98}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/9887022}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=9887022}, day = {1}, journal = {Am J Physiol Heart Circ Physiol}, keywords = {electrophysiology, human}, month = {January}, number = {1}, pages = {H98--106}, posted-at = {2007-08-03 12:16:20}, priority = {4}, title = {Transmembrane ICa contributes to rate-dependent changes of action potentials in human ventricular myocytes}, url = {http://ajpheart.physiology.org/cgi/content/abstract/276/1/H98}, volume = {276}, year = {1999} }

TY - JOUR ID - citeulike:1533174 L3 - citeulike-article-id:1533174 N2 - The mechanism of action potential abbreviation caused by increasing rate in human ventricular myocytes is unknown. The present study was designed to determine the potential role of Ca2+ current (ICa) in the rate-dependent changes in action potential duration (APD) in human ventricular cells. Myocytes isolated from the right ventricle of explanted human hearts were studied at 36{degrees}C with whole cell voltage and current-clamp techniques. APD at 90% repolarization decreased by 36 {+/-} 4% when frequency increased from 0.5 to 2 Hz. Equimolar substitution of Mg2+ for Ca2+ significantly decreased rate-dependent changes in APD (to 6 {+/-} 3%, P < 0.01). Peak ICa was decreased by 34 {+/-} 3% from 0.5 to 2 Hz (P < 0.01), and ICa had recovery time constants of 65 {+/-} 12 and 683 {+/-} 39 ms at [-]80 mV. Action potential clamp demonstrated a decreasing contribution of ICa during the action potential as rate increased. The rate-dependent slow component of the delayed rectifier K+ current (IKs) was not observed in four cells with an increase in frequency from 0.5 to 3.3 Hz, perhaps because the IKs is so small that the increase at a high rate could not be seen. These results suggest that reduction of Ca2+ influx during the action potential accounts for most of the rate-dependent abbreviation of human ventricular APD. IS - 1 JF - Am J Physiol Heart Circ Physiol EP - 106 TI - Transmembrane ICa contributes to rate-dependent changes of action potentials in human ventricular myocytes VL - 276 SP - H98 KW - electrophysiology KW - human AU - Li, Gui-Rong AU - Yang, Baofeng AU - Feng, Jianlin AU - Bosch, Ralph AU - Carrier, Michel AU - Nattel, Stanley PY - 1999/01/01/ UR - http://ajpheart.physiology.org/cgi/content/abstract/276/1/H98 ER -