These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Properties of intracellular calcium stores and their role in receptor-mediated catecholamine secretion in rat adrenal chromaffin cells.
    Author: Warashina A, Fujiwara N.
    Journal: Biol Signals; 1995; 4(4):195-205. PubMed ID: 8720686.
    Abstract:
    Simulation of rat adrenal chromaffin cells either with receptor agonists such as muscarine, bradykinin and histamine or with caffeine in Ca(2+)-free Krebs solution induced a brief increase in the intracellular free Ca2+ concentration, [Ca2+]i, which terminated within 90 s. Both the agonist- and caffeine-induced [Ca2+]i responses were abolished in cells which had been treated with either 500 nM thapsigargin (TG) or 20 microM ryanodine, suggesting that inositol trisphosphate and caffeine cause Ca2+ release either from the same Ca2+ store or from distinct stores which exchange Ca2+ rapidly. In normal Krebs solution, these agonists evoked catecholamine (CA) secretion which showed an initial transient followed by a sustained component. Neither component of the secretion was significantly affected by TG or ryanodine. In the medium containing 16 microM Ca2+ or no Ca2+, CA secretion evoked by 30-second stimulation with 100 microM muscarine was 59 or 7%, respectively, of that evoked in the normal medium containing 2 mM Ca2+. In TG-treated cells, the CA secretion at 16 microM Ca2+ was reduced to 23% and that in the Ca(2+)-free medium was completely abolished. These results suggest that the receptor-mediated Ca2+ entry solely determines the rate of CA secretion in rat chromaffin cells when stimulated by receptor agonists in the normal medium, whereas intracellular Ca2+ release and Ca2+ entry may cooperatively support the secretion when cells are stimulated in media containing low concentrations of Ca2+.
    [Abstract] [Full Text] [Related] [New Search]