L-type and dihydropyridine-resistant calcium channel trigger exocytosis with similar efficacy in single rat pancreatic beta cells

Biochem Biophys Res Commun. 1998 Feb 24;243(3):878-84. doi: 10.1006/bbrc.1998.8197.

Abstract

The relationship between depolarization-induced exocytosis and inward Ca2+ current (Ica) in single isolated rat pancreatic beta cells was investigated in perforated patch recordings. Ica was elicited by depolarization and change in cell membrane capacitance (Cm) was monitored as an indicator of resultant exocytosis. While there was significant variety of change in Cm and Ca2+ influx, the increase in Cm had positive correlation with Ca2+ influx and also with duration of depolarization. Removal of extracellular Ca2+ or inclusion of extracellular Cd2+ (100 microM) completely eliminated both Ica and increase in Cm following depolarization. Dihydropyridine (DHP) Ca2+ channel blocker (5 microM) partly and in parallel suppressed depolarization-induced peak Ica, Ca2+ influx, and change in Cm. These data suggest that rat pancreatic beta cell expresses at least two types of Ca2+ channels; Ca2+ entry through these DHP-sensitive, presumably L-type, and DHP-insensitive channels triggers exocytosis with similar efficacy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cadmium / pharmacology
  • Calcium / administration & dosage
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / physiology*
  • Cells, Cultured
  • Dihydropyridines / pharmacology*
  • Drug Resistance
  • Electric Conductivity
  • Exocytosis*
  • Islets of Langerhans / physiology*
  • Nicardipine / pharmacology
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Dihydropyridines
  • Cadmium
  • 1,4-dihydropyridine
  • Nicardipine
  • Calcium