KCl-induced insulin secretion from RINm5F cells is mediated through Ca influx along L-type Ca channels.

Autor: Roenfeldt, M., Safayhi, H., Ammon, H.P.T.
Zdroj: Naunyn-Schmiedeberg's Archives of Pharmacology; 1992, Vol. 346 Issue 5, p527-531, 5p
Abstrakt: In order to characterize the voltage-dependent Ca channels of insulin secretory RINm 5F cells, we have studied the binding of the dihydropyridine (DHP) type Ca antagonist PN 200-110 and its effect on insulin release. In the membrane preparation from RINm 5F cells [H]-(+)-PN 200-110 bound to a high affinity binding site in a stereoselective manner (KD: 7.0 n M, B: 858 fmol/mg protein). The benzothiazepine type Ca antagonist D- cis-diltiazem increased the binding of [H]-(+)-PN 200-110 in a temperature-dependent manner. The phenylalkylamine-type Ca antagonist verapamil decreased PN binding with an IC of 100 μ M. (+)-PN 200-110 inhibited KCl-(25 m M)-induced insulin release (IC = 10 n M), Effects on binding and hormone release occurred over comparable concentration ranges: 1 μ M PN 200-110 produced 100% displacement and totally abolished depolarization-mediated insulin release. The N-type Ca-antagonist ω-conotoxin showed no effect on KCl-induced insulin release. The data suggest that in RINm 5 F cells only l-type Ca channels are involved in the mechanism of depolarization-mediated insulin release. [ABSTRACT FROM AUTHOR]
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