© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Stimulation of L-type Ca2+ current in human atrial myocytes by insulin
aMedizinische Universitätsklinik Würzburg, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany
bPhysiologische Chemie II, Theodor-Boveri-Institut für Biowissenschaften, Würzburg, Germany
cKlinik und Poliklinik für Herz- und Thoraxchirurgie der Universität Würzburg, Josef-Schneider-Strasse 6, 97080 Würzburg, Germany
* Corresponding author. Tel.: +49-931-201-2775; fax: +49-931-201-2775 s.maier{at}medizin.uni-wuerzburg.de
Objective: The L-type calcium current (ICa,L) in isolated human atrial myocytes was investigated as a possible target of insulin in the regulation of cardiac function. Methods: Atrial myocytes were obtained from patients undergoing cardiac surgery. Using the whole-cell configuration of the patch-clamp technique, we investigated the stimulation of ICa,L by insulin in single human atrial myocytes. Results: We found a dose-dependent stimulation of ICa,L by insulin at concentrations of 100 nM, 1 µM and 10 µM. Maximum stimulation of ICa,L over basal ICa,L was 140±12% (n=11) at 10 µM insulin. The maximum conductance of ICa,L was increased by 10 µM insulin from 4.0±0.3 nS to 8.3±1.0 nS (n=6). The stimulation of ICa,L by insulin was dose-dependent and reversible. Isoproterenol (10 nM) that stimulates ICa,L by 271±48% (n=10) over basal ICa,L acted faster than insulin. The half-maximum stimulation of ICa,L by isoproterenol and insulin (10 µM) was reached after 31±2 s and 52±5 s, respectively. The insulin effect shown was totally reversed by acetylcholine (3 µM) which is known to inhibit adenylyl cyclase activity/cAMP-production via Gi-proteins. Also, the selective insulin receptor tyrosine kinase inhibitor (hydroxy-2-naphthanelyl-methyl)phosphonic acid completely inhibited the insulin induced effect. Conclusion: Our data show that insulin stimulates the L-type calcium current in isolated human atrial myocytes in a dose-dependent and reversible manner which appears to involve the insulin receptor tyrosine kinase. Insulin regulation of ICa,L in human atrial myocytes may be an interesting system for the analysis of the metabolic syndrome in man.
KEYWORDS Acetylcholine; Ca-channel; Diabetes, G-proteins, Hormones
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