| Literature DB >> 12479228 |
J P Bénitah1, A M Gómez, J Fauconnier, B G Kerfant, E Perrier, G Vassort, S Richard.
Abstract
The L-type Ca2+ current (I(Ca-L)) plays a key role in the cardiac excitation-contraction (E-C) coupling. Thus, it is a major target for many transmitters and hormones modulating cardiac function and, therefore, for pharmacological drugs to regulate inotropy. Ca2+ (and other) ion currents are commonly studied in animal tissues for practical reasons. Investigations in human cardiomyocytes started extensively only ten years ago with the development of patch-clamp techniques, enzymatic cell dissociation procedures, and surgical techniques. These studies have already provided valuable information concerning the nature, biophysics, pharmacology and regulation of human cardiac ionic currents in normal and diseased tissues. Interesting advances have been made to understand the role of I(Ca-L) in the development of chronic atrial fibrillation (AF). Alterations of single channel activity and regulation of macroscopic I(Ca-L) have also been found in heart failure (HF), ugh some of the data are divergent and puzzling. The T-type Ca2+ current (I(Ca-T)) has never been recorded in human cardiomyocytes. After a rapid overview of the basic properties of human cardiac Ca2+ currents, we focus on selected aspects of pathophysiology that are still unsolved.Entities:
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Year: 2002 PMID: 12479228 DOI: 10.1007/s003950200023
Source DB: PubMed Journal: Basic Res Cardiol ISSN: 0300-8428 Impact factor: 17.165