Protein kinase C activator inhibits voltage-sensitive Ca2+ channels and catecholamine secretion in adrenal chromaffin cells

FEBS Lett. 1995 Feb 13;359(2-3):137-41. doi: 10.1016/0014-5793(95)00026-6.

Abstract

We have investigated the effects of the phorbol ester 12-myristate 13-acetate (PMA) on depolarization-evoked Ca2+ influx and catecholamine secretion in bovine adrenal chromaffin cells. PMA (100 nM) strongly inhibited K(+)-evoked [Ca2+]i transients and Mn2+ quenching of fura-2 fluorescence. In contrast, 4 alpha-phorbol 12,13-didecanoate, a phorbol ester inactive on protein kinase C (PKC), had no effect. Maximal PMA-mediated inhibition occurred at 5-10 min incubations and were variable from cell to cell, ranging from 25 to 65% of controls. The [Ca2+]i transients evoked by the L-type Ca2+ channel activator Bay K 8644 were strongly inhibited by 100 nM PMA. PMA (0.1-10 microM) inhibited K(+)-evoked adrenaline and noradrenaline release by 23-44%. The data indicate that phorbol ester-mediated activation of PKC inhibits voltage-sensitive Ca2+ channels in chromaffin cells, leading to a prominent depression of depolarization-evoked catecholamine secretion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenal Cortex / drug effects*
  • Adrenal Cortex / enzymology
  • Adrenal Cortex / metabolism
  • Animals
  • Calcium / metabolism
  • Calcium Channel Blockers / pharmacology*
  • Catecholamines / metabolism*
  • Cattle
  • Electrophysiology
  • In Vitro Techniques
  • Manganese / metabolism
  • Protein Kinase C / metabolism*
  • Tetradecanoylphorbol Acetate / pharmacology*

Substances

  • Calcium Channel Blockers
  • Catecholamines
  • Manganese
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate
  • Calcium