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Ca2+ channel inhibition induced by nitric oxide in rat insulinoma RINm5F cells

C Grassi1, M D'Ascenzo, A Valente

  • 1Institute of Human Physiology, Catholic University S. Cuore, Largo F. Vito 1, I-00168 Rome, Italy. claudiograssi@hotmail.com

Pflugers Archiv : European Journal of Physiology
|February 4, 1999
PubMed

Insights

Nitric oxide (NO) donors inhibit high-voltage-activated calcium channels in insulin-secreting cells. This NO-induced inhibition, likely mediated by cyclic GMP, affects hormone and neurotransmitter release.

Area of Science:

  • Cellular physiology
  • Neuroendocrinology
  • Ion channel research

Background:

  • High-voltage-activated calcium channels are crucial for hormone and neurotransmitter release.
  • Nitric oxide (NO) is a signaling molecule with diverse physiological roles.
  • The precise mechanisms of NO action on calcium channels in secretory cells require further elucidation.

Purpose of the Study:

  • To investigate the effects of nitric oxide (NO) donors on high-voltage-activated calcium channels in insulin-secreting RINm5F cells.
  • To determine the signaling pathways involved in NO-mediated channel modulation.
  • To assess the potential impact of NO on hormone and neurotransmitter release.

Main Methods:

  • Patch-clamp electrophysiology in whole-cell configuration was used to measure Ba2+ currents.
  • RINm5F cells, a rat insulinoma cell line, served as the model system.
  • Various NO donors, scavengers, and pathway inhibitors were employed to dissect the NO signaling cascade.

Main Results:

  • Sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) dose-dependently inhibited Ba2+ currents.
  • The NO scavenger carboxy-PTIO attenuated SNP-induced inhibition, indicating NO dependence.
  • 8-bromoguanosine 3':5'-cyclic monophosphate (8-Br-cGMP) mimicked SNP's inhibitory effects.
  • Inhibition of soluble guanylyl cyclase with ODQ reduced SNP's effect.
  • SNP inhibited both L-type and P/Q-type calcium channels.

Conclusions:

  • Nitric oxide (NO) inhibits high-voltage-activated calcium channels in RINm5F cells.
  • The inhibitory mechanism likely involves an increase in intracellular cyclic GMP (cGMP) levels.
  • NO-mediated modulation of calcium channels may significantly influence hormone and neurotransmitter secretion.

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