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Volume 270, Number 29, Issue of July 21, pp. 17361-17367, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.

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(Received for publication, February 21, 1995; and in revised form, May 9, 1995)

From the  (1)Groupe d'Electrophysiologie Moléculaire, Centre de Physiologie et Physiophathologie Cellulaire, Université Joseph Fourier, BP 53X, F-38041 Grenoble Cedex, France and (2)INSERM Unité 244, Commissariat l'Energie Atomique, Département de Biologie Moléculaire et Structurale, Centre d'Etudes Nucleaires, F-38054 Grenoble Cedex 9, France

Basic fibroblast growth factor (bFGF) is a potent mitogen for many cell lineages including fetal cardiomyocytes. Furthermore, bFGF has been shown to modify gene expression, in vitro, in adult nonproliferative ventricular myocytes. This effect is suspected to be partly responsible for the genetic modifications that occur in vivo under pathophysiological conditions such as ischemia or pressure overload and that lead to myocardial hypertrophy. However, little is known about the first steps of the molecular mechanisms that take place soon after cell activation by bFGF. In this study, using biochemical and electrophysiological approaches, we have established, on cardiomyocytes cultured from neonatal rat ventricles, that (i) differentiated beating cells express at least two classes of bFGF-receptors having high and low affinity (K = 10 ± 2 pM and 1 ± 0.5 nM); (ii) the stimulation of these bFGF receptors promotes an increase in the beating frequencies of cultured cardiomyocytes (40 ± 10%); (iii) bFGF provokes the activation of poorly specific and voltage-independent calcium channels (12pS); (iv) inositol 1,4,5-trisphosphate enhances similar bFGF-induced Ca currents and is therefore suspected to be a second messenger triggering this activation. These results support the presence, in cultured cardiomyocytes, of new calcium channels whose activation after bFGF binding may be partly responsible for the cell response to this growth factor.

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