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   <subfield code="a">KCl-induced insulin secretion from RINm5F cells is mediated through Ca2+ influx along L-type Ca2+ channels</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[M. Roenfeldt, H. Safayhi, H.P.T. Ammon]</subfield>
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   <subfield code="a">Summary: In order to characterize the voltage-dependent Ca2+ channels of insulin secretory RINm 5F cells, we have studied the binding of the dihydropyridine (DHP) type Ca2+ antagonist PN 200-110 and its effect on insulin release. In the membrane preparation from RINm 5F cells [3H]-(+)-PN 200-110 bound to a high affinity binding site in a stereoselective manner (KD: 7.0 nM, Bmax: 858 fmol/mg protein). The benzothiazepine type Ca2+ antagonist D-cis-diltiazem increased the binding of [3H]-(+)-PN 200-110 in a temperature-dependent manner. The phenylalkylamine-type Ca2+ antagonist verapamil decreased PN binding with an IC50 of 100 μM. (+)-PN 200-110 inhibited KCl-(25 mM)-induced insulin release (IC50 = 10 nM), Effects on binding and hormone release occurred over comparable concentration ranges: 1 μM PN 200-110 produced 100% displacement and totally abolished depolarization-mediated insulin release. The N-type Ca2+-antagonist ω-conotoxin showed no effect on KCl-induced insulin release. The data suggest that in RINm 5 F cells only l-type Ca2+ channels are involved in the mechanism of depolarization-mediated insulin release.</subfield>
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   <subfield code="a">Calcium channel</subfield>
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   <subfield code="D">M.</subfield>
   <subfield code="u">Department of Pharmacology, Institute of Pharmaceutical Sciences, University of Tübingen, Auf der Morgenstelle 8, W-7400, Tübingen, Federal Republic of Germany</subfield>
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