Role of calcium in thyrotrophin-releasing hormone-stimulated release of melanocyte-stimulating hormone from frog neurointermediate lobe

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Abstract
The effect of modifications of extracellular calcium concentrations on α-MSH release has been studied using perifused frog neurointermediate lobes. Increasing concentrations of calcium (from 2 to 10 mmol/l) gave rise to a dose-related stimulation of α-MSH secretion, whereas reduction of Ca2+ from 2 to 15 mmol/l partially inhibited α-MSH release. The direct effect of extracellular Ca2+ on α-MSH secretion was confirmed by the dose-dependent stimulation of α-MSH release induced by the calcium ionophore A23187. Perifusion with a calcium-free medium or blockade of Ca2+ channels by 4 mmol Co2+/l both resulted in an inhibition of spontaneous and TRH-induced α-MSH release. Conversely, administration of verapamil or methoxy-verapamil (10 μmol/l each) did not alter basal secretion and had no effect on the response of the glands to TRH. Nifedipine (10 μmol/l), which was able to block KCl (20 mmol/l)-evoked α-MSH release, induced a slight inhibition of basal α-MSH secretion, indicating that extracellular Ca2+ levels may regulate α-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels. In contrast TRH-induced α-MSH release was not affected by nifedipine or dantrolene (10 μmol/l), and BAY-K-8644 (1 μmol/l) did not significantly modify the response of neurointermediate lobes to TRH. Taken together, these results suggest that TRH-induced α-MSH secretion is associated with calcium influx across the plasma membrane and that calcium entry caused by TRH may occur through nifedipine/verapamil-insensitive Ca2+ channels.

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