Role of T-type Ca2+ channels in the heart

After the first demonstration 30 years ago that Ca2+ could permeate through two different channels, the occurrence and role of T-type Ca2+ current, ICaT have been the matter of hundreds of publications, including the two 1985’ reports in various cardiac tissues and species. Except for its specific biophysical characteristics, ICaT is no longer so easily distinguished from the L-type Ca2+ current, ICaL, since it is also sensitive to multiple compounds and various neuromediators including the β-adrenergic agonists. Changes in ICaT occur during development, so that while it is recorded in all embryonic and neonatal cells investigated, ICaT has been reported in adult ventricular cells of only few species in control. However, under various pathological conditions, ICaT is often recorded at some phases of remodelling at least in some localized area and one or more of the three channel proteins, Cav3.1–3.3 are clearly re-expressed under the influence of IGF-1, endothelin, and angiotensin II. ICaT contributes to the control of electrical activity including pacemaker and arrhythmia. Furthermore ICaT, and its low-depolarisation window current, participate in Ca2+ entry, so that ICaT has been involved in the release of Ca2+ from internal stores, the Ca2+-induced Ca2+ release mechanism, although at much lower level than ICaL. ICaT contributes also to Ca2+-dependent hormonal secretion. This review further emphasizes the difficulties encountered in analysing this current.