Nitric oxide induces [Ca2+]i oscillations in pituitary GH3 cells

Involvement of IDR and ERG K + currents

Agnese Secondo, Anna Pannaccione, Mauro Cataldi, Rossana Sirabella, Luigi Formisano, Gianfranco Di Renzo, Lucio Annunziato

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The role of nitric oxide (NO) in the occurrence of intracellular Ca 2+ concentration ([Ca2+]i) oscillations in pituitary GH3 cells was evaluated by studying the effect of increasing or decreasing endogenous NO synthesis with L-arginine and nitro-L-arginine methyl ester (L-NAME), respectively. When NO synthesis was blocked with L-NAME (1 mM) [Ca2+]i, oscillations disappeared in 68% of spontaneously active cells, whereas 41% of the quiescent cells showed [Ca2+]i oscillations in response to the NO synthase (NOS) substrate L-arginine (10 mM). This effect was reproduced by the NO donors NOC-18 and S-nitroso-N-acetylpenicillamine (SNAP). NOC-18 was ineffective in the presence of the L-type voltage-dependent Ca2+ channels (VDCC) blocker nimodipine (1 μM) or in Ca2+-free medium. Conversely, its effect was preserved when Ca2+ release from intracellular Ca2+ stores was inhibited either with the ryanodine-receptor blocker ryanodine (500 μM) or with the inositol 1,4,5-trisphosphate receptor blocker xestospongin C (3 μM). These results suggest that NO induces the appearance of [Ca2+]i oscillations by determining Ca2+ influx. Patch-clamp experiments excluded that NO acted directly on VDCC but suggested that NO determined membrane depolarization because of the inhibition of voltage-gated K+ channels. NOC-18 and SNAP caused a decrease in the amplitude of slow-inactivating (IDR) and ether-à-go-go-related gene (ERG) hyperpolarization-evoked, deactivating K+ currents. Similar results were obtained when GH3 cells were treated with L-arginine. The present study suggests that in GH3 cells, endogenous NO plays a permissive role for the occurrence of spontaneous [Ca2+]i oscillations through an inhibitory effect on IDR and on I ERG.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume290
Issue number1
DOIs
Publication statusPublished - Jan 2006

Fingerprint

Nitric Oxide
Arginine
S-Nitroso-N-Acetylpenicillamine
Voltage-Gated Potassium Channels
Inositol 1,4,5-Trisphosphate Receptors
Ryanodine
Nimodipine
Ryanodine Receptor Calcium Release Channel
Nitric Oxide Donors
Depolarization
Clamping devices
Electric potential
Nitric Oxide Synthase
Ether
Genes
Membranes
Substrates
NOC 18
Experiments
arginine methyl ester

Keywords

  • Ether-à-go-go-related gene potassium channels
  • Fast-inactivating outward currents
  • Slow-inactivating outward currents
  • Voltage-gated potassium channels

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Nitric oxide induces [Ca2+]i oscillations in pituitary GH3 cells : Involvement of IDR and ERG K + currents. / Secondo, Agnese; Pannaccione, Anna; Cataldi, Mauro; Sirabella, Rossana; Formisano, Luigi; Di Renzo, Gianfranco; Annunziato, Lucio.

In: American Journal of Physiology - Cell Physiology, Vol. 290, No. 1, 01.2006.

Research output: Contribution to journalArticle

Secondo, Agnese ; Pannaccione, Anna ; Cataldi, Mauro ; Sirabella, Rossana ; Formisano, Luigi ; Di Renzo, Gianfranco ; Annunziato, Lucio. / Nitric oxide induces [Ca2+]i oscillations in pituitary GH3 cells : Involvement of IDR and ERG K + currents. In: American Journal of Physiology - Cell Physiology. 2006 ; Vol. 290, No. 1.
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