Tags

Type your tag names separated by a space and hit enter

Propafenone inhibition of human atrial myocyte repolarizing currents.
J Mol Cell Cardiol. 1998 Apr; 30(4):783-93.JM

Abstract

This study was aimed at defining cellular electropharmacologic effects of propafenone on repolarizing currents in human atrial myocytes. Whole-cell patch-clamp of enzymatically isolated atrial myocytes from 11 cardiac surgical patients aged between 29 days and 74 years revealed potent time- and concentration-dependent (IC50 = 4.8 +/- 0.4 mumol/l), but age-, voltage-, and frequency-independent propafenone inhibition of transient outward current. Time course of apparent transient outward current inactivation was best described by a single exponential process in the absence of propafenone and by a double exponential model in its presence, with drug-concentration-dependent acceleration of the fast exponential component. Neither voltage dependence of steady-state transient outward current inactivation nor time course of recovery from inactivation was affected by propafenone. Significant inhibition (P < 0.05) of the ultra-rapidly activating delayed rectifier and inwardly rectifying currents was observed only in the presence of > or = 10 mumol/l propafenone. These actions of propafenone could explain its repolarization prolonging effect and might contribute to clinical electrophysiologic responses which have been documented in patients of all ages.

Authors+Show Affiliations

Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9602427

Citation

Gross, G J., and N A. Castle. "Propafenone Inhibition of Human Atrial Myocyte Repolarizing Currents." Journal of Molecular and Cellular Cardiology, vol. 30, no. 4, 1998, pp. 783-93.
Gross GJ, Castle NA. Propafenone inhibition of human atrial myocyte repolarizing currents. J Mol Cell Cardiol. 1998;30(4):783-93.
Gross, G. J., & Castle, N. A. (1998). Propafenone inhibition of human atrial myocyte repolarizing currents. Journal of Molecular and Cellular Cardiology, 30(4), 783-93.
Gross GJ, Castle NA. Propafenone Inhibition of Human Atrial Myocyte Repolarizing Currents. J Mol Cell Cardiol. 1998;30(4):783-93. PubMed PMID: 9602427.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Propafenone inhibition of human atrial myocyte repolarizing currents. AU - Gross,G J, AU - Castle,N A, PY - 1998/5/29/pubmed PY - 1998/5/29/medline PY - 1998/5/29/entrez SP - 783 EP - 93 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 30 IS - 4 N2 - This study was aimed at defining cellular electropharmacologic effects of propafenone on repolarizing currents in human atrial myocytes. Whole-cell patch-clamp of enzymatically isolated atrial myocytes from 11 cardiac surgical patients aged between 29 days and 74 years revealed potent time- and concentration-dependent (IC50 = 4.8 +/- 0.4 mumol/l), but age-, voltage-, and frequency-independent propafenone inhibition of transient outward current. Time course of apparent transient outward current inactivation was best described by a single exponential process in the absence of propafenone and by a double exponential model in its presence, with drug-concentration-dependent acceleration of the fast exponential component. Neither voltage dependence of steady-state transient outward current inactivation nor time course of recovery from inactivation was affected by propafenone. Significant inhibition (P < 0.05) of the ultra-rapidly activating delayed rectifier and inwardly rectifying currents was observed only in the presence of > or = 10 mumol/l propafenone. These actions of propafenone could explain its repolarization prolonging effect and might contribute to clinical electrophysiologic responses which have been documented in patients of all ages. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/9602427/Propafenone_inhibition_of_human_atrial_myocyte_repolarizing_currents_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(98)90643-5 DB - PRIME DP - Unbound Medicine ER -