Mechanism of arginine-stimulated Ca2+ influx into pancreatic B cell

Am J Physiol. 1984 Jan;246(1 Pt 1):E38-43. doi: 10.1152/ajpendo.1984.246.1.E38.


The mechanism by which arginine stimulates Ca2+ inflow into the pancreatic B cell was investigated. Arginine (10 mM) increased 86Rb outflow from perifused rat pancreatic islets, suggesting that arginine-stimulated Ca2+ influx into the B cell does not result from a decrease in K+ conductance. Arginine stimulated Ca2+ uptake in isolated islets over short incubation periods and increased 45Ca outflow from perifused islets in a Ca2+-dependent manner. The calcium channel blocker verapamil inhibited both arginine-stimulated 45Ca uptake and 45Ca outflow. However, the sensitivity toward verapamil of arginine-stimulated islets was lower than that of islets stimulated by 20 mM K+, which gates voltage-sensitive Ca2+ channels. It was similar to that of islets stimulated by 8.3 mM glucose, which is thought to mainly gate voltage-insensitive Ca2+ channels. It is suggested that arginine stimulates Ca2+ inflow into the B cell by gating voltage-insensitive Ca2+ channels. The arginine-induced stimulation of Ca2+ inflow could participate in the depolarizing action of the amino acid on the B cell membrane.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arginine / pharmacology*
  • Calcium / metabolism*
  • In Vitro Techniques
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Kinetics
  • Potassium / pharmacology
  • Rats
  • Rubidium / metabolism
  • Verapamil / pharmacology


  • Ion Channels
  • Arginine
  • Verapamil
  • Rubidium
  • Potassium
  • Calcium