POSSIBLE INVOLVEMENT OF INTRACELLULAR CA2-EVOKED CATECHOLAMINE RELEASE FROM ADRENAL CHROMAFFIN CELLS( IN HYPOSMOSIS)

Citation
K. Morita et al., POSSIBLE INVOLVEMENT OF INTRACELLULAR CA2-EVOKED CATECHOLAMINE RELEASE FROM ADRENAL CHROMAFFIN CELLS( IN HYPOSMOSIS), Neurochemistry international, 31(5), 1997, pp. 731-737
Citations number
23
Categorie Soggetti
Biology,Neurosciences
ISSN journal
01970186
Volume
31
Issue
5
Year of publication
1997
Pages
731 - 737
Database
ISI
SICI code
0197-0186(1997)31:5<731:PIOICC>2.0.ZU;2-2
Abstract
The influence of hyposmotic conditions on catecholamine release was st udied using cultured adrenal chromaffin cells. Incubation of the cells in hyposmotic solution led to the enhancement of catecholamine releas e in a manner dependent on the reduction of osmolarity. Hyposmosis-evo ked catecholamine release was similarly observed in the presence or ab sence of extracellular Ca2+, and was not significantly affected by org anic and inorganic Ca2+ entry blockers. These results indicated that t he hyposmosis-evoked release might be associated with a rise in the in tracellular Ca2+ concentration. Further studies showed that neither ry anodine nor thapsigargin caused any significant effect on hyposmosis-e voked catecholamine release, whereas pretreatment of chromaffin cells with carbonyl cyanide m-chlorophenyl hydrazone significantly enhanced the hyposmosis-evoked release. Catecholamine release evoked by exposur e to hyposmotic medium is therefore thought to be mediated through int racellular Ca2+, which may be mainly sequestered by the mitochondrial pools. Neither caffeine-nor inositol 1,4,5-trisphosphate-sensitive Ca2 + pools seems likely to be involved in hyposmosis-evoked catecholamine release, although the Ca2+ pools that contribute to the elevation of intracellular Ca2+ observed under hyposmotic conditions are not yet co mpletely identified. (C) 1997 Elsevier Science Ltd.