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1 Physiopathologie des Canaux Ioniques, Institut de Génétique Humaine-Centre National de la Recherche Scientifique (CNRS) UPR 1142, 34396 Montpellier cedex 05; and 2 Biologie des Neurones Endocrines, Centre CNRS-INSERM de Pharmacologie Expérimentale-CNRS UMR 5101, 34094 Montpellier cedex 05, France
T-type
Ca2+ channels have been suggested to play a role in
cardiac automaticity, cell growth, and cardiovascular remodeling. Although three genes encoding for a T-type Ca2+ channel
have been identified, the nature of the isoform(s) supporting the
cardiac T-type Ca2+ current (ICa,T)
has not yet been determined. We describe the postnatal evolution of
ICa,T density in freshly dissociated rat atrial
and ventricular myocytes and its functional properties at peak current
density in young atrial myocytes. ICa,T displays a classical low activation threshold, rapid inactivation kinetics, negative steady-state inactivation, slow deactivation, and the presence
of a window current. Interestingly, ICa,T is
poorly sensitive to Ni2+ and insensitive to R-type current
toxin SNX-482. RT-PCR experiments and comparison of functional
properties with recombinant Ca2+ channel subtypes suggest
that neonatal ICa,T is related to the 
1G-subunit. Atrial natriuretic factor (ANF) secretion
was measured using peptide radioimmunoassays in atrial tissue.
Pharmacological dissection of ANF secretion indicates an important
contribution of ICa,T to Ca2+
signaling during the neonatal period.
cardiac myocytes; atrial natriuretic factor; electrophysiology
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