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
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.