Endothelin evoked Ca2+ transients and oscillations in A10 vascular smooth muscle cells.

Endothelin (200 nM) evoked a rapid rise in [Ca2+]i which was then followed by a maintained elevation of [Ca2+]i. The initial transient can be explained by the release of stored Ca2+ whilst the maintained plateau is likely to be an influx of Ca2+ as it was partially inhibited by nifedipine (5 microM) and the remaining component abolished by the removal of extracellular Ca2+. Vasopressin (1 nM) evoked a similar response which also showed a nifedipine insensitive component to it's plateau phase. Endothelin also evoked oscillations in [Ca2+]i; these where characterised by a rapid rising phase followed by a slower decline, with no 'pacemaker' rise in [Ca2+]i preceding the rising phase. The oscillations were inhibited by the addition of 5 microM nifedipine or the removal of extracellular Ca2+ suggesting they are at least in part dependent on voltage gated Ca2+ entry.