Regulation of Ca2+ influx by a protein kinase C activator in chromaffin cells: differential role of P/Q- and L-type Ca2+ channels
| Autor: | Luis M. Rosario, Michael R. Boarder, Rosa M. Santos, Cristina M. Sena |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Phorbol ester
medicine.medical_specialty Chromaffin Cells Spider Venoms Fluorescence chemistry.chemical_compound omega-Agatoxin IVA Nitrendipine Protein kinase C omega-Conotoxin GVIA Internal medicine medicine Animals Adrenal medulla chromaffin cell Omega-Conotoxin GVIA Ca2+ channel voltage-sensitive Protein kinase A Protein Kinase C Pharmacology Manganese Dose-Response Relationship Drug Voltage-dependent calcium channel Calcium Channel Blockers Staurosporine Molecular biology Enzyme Activation Ca2+ concentration cytosolic free medicine.anatomical_structure Endocrinology chemistry Ionomycin Chromaffin cell Carcinogens Potassium Phorbol Tetradecanoylphorbol Acetate Calcium Cattle Calcium Channels Fura-2 Peptides medicine.drug |
| Zdroj: | Repositório Científico de Acesso Aberto de Portugal Repositório Científico de Acesso Aberto de Portugal (RCAAP) instacron:RCAAP |
| ISSN: | 0014-2999 |
| DOI: | 10.1016/s0014-2999(98)00908-x |
| Popis: | Phorbol esters reduce depolarization-evoked Ca2+ influx in adrenal chromaffin cells, suggesting that voltage-sensitive Ca2+ channels (VSCCs) are inhibited by protein kinase C-mediated phosphorylation. We now address the possibility that L- and P/Q-type Ca2+ channel subtypes might be differentially involved in phorbol ester action. In bovine chromaffin cells, short-term (10 min) incubations with phorbol 12-myristate 13-acetate (PMA) inhibited early high K+-evoked rises in cytosolic free Ca2+ concentration ([Ca2+]i) and the early component of the depolarization-evoked Mn2+ quenching of fura-2 fluorescence in a dose-dependent manner (IC50: 18 and 7 nM; maximal inhibitions: 45 and 48%, respectively). The protein kinase C inhibitor staurosporine (100 nM) reverted the inhibitory action of PMA. PMA (0.1-1 [mu]M) inhibited the early and late phases of the ionomycin (2 [mu]M)-evoked [Ca2+]i transients by 14-23%. [omega]-Agatoxin IVA, a blocker of P/Q-type Ca2+ channels, inhibited high K+-evoked [Ca2+]i rises in a dose-dependent fashion (IC50=50 nM). In contrast, 0.1 [mu]M [omega]-conotoxin GVIA, a blocker of N-type channels, was without effect. A sizeable ( |
| Databáze: | OpenAIRE |
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