― The involvement of different types of voltage-dependent calcium channels (VDCC) in the stimulatory action of GnRH (in comparison with K+) on maturational gonadrotropin (GtH) release was investigated using superfused carp pituitary cells.Theaction of these 2 stimulants was not mod- ified either by D600 or nifedipine (drugs blocking L-type of VDCC).Cadmium (Cd 2+ ), which blocks all types of VDCC indifferently, provoked a dose-dependent stimulation of GtH secretion.Cd 2+ action was not altered by addition of sGnRH in any of the doses.Similar results were obtained using K• as a secretagogue, but only the highest dose of Cd 2 + (200 I1molll) was able to completely block K + ac- tion.Low doses (0.1 and 1 I1 molll) of the L-type VDCC activator BAY-K8644 did not change basal GtH secretion and had no effect on sGnRH-stimulated GtH secretion.Surprisingly, doses (10 I1molll and higher) of BAY-K8644 evoked dose-dependent inhibition of GtHsecretion.On the other hand, a higher concentration (20 pmol/I) of nifedipine provoked a stimulation of GtH release.Our results indicate that the stimulatory action of GnRH and K + involves activation of a certain type of cadmium-sensitive VDCC (probably T-or N-type VDCC) whereas dihydropyridine and di- phenylalkylamine sensitive VDCC (L-type VDCC) does not participate in this phenomenon.The in- hibitory action of BAY-K8644 and, on the other hand, the stimulatory action of nifedipine indicate that L-type VDCC probably play a role in other physiological pathways regulating GtH release in carp.GnRN et de K + implique l'activation de certains types de VDCC sensibles au cadmium, sans doute de type T ou N, les canaux sensibles aux dihydropiridine et diphényloalkylamine, de type L, n'étant pas mis en jeu dans ces phénomènes.Les actions inhibitrices du BAY K8644, et stimulatrice de la ni- fedipine, montrent cependant que les canaux de type L jouent sans doute un rôle dans d'autres mé- canismes régulant la sécrétion de GtH.
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Mikołajczyk et al. (1990) studied this question.
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