Premium
Sodium Fluoride Mimics the Effect of Prostaglandin E 2 on Catecholamine Release from Bovine Adrenal Chromaffin Cells
Author(s) -
Ito Seiji,
Negishi Manabu,
MochizukiOda Noriko,
Yokohama Hiromitsu,
Hayaishi Osamu
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb02560.x
Subject(s) - endocrinology , catecholamine , medicine , inositol phosphate , chromaffin cell , ouabain , chemistry , sodium fluoride , inositol , inositol trisphosphate , adrenal medulla , prostaglandin e , stimulation , receptor , sodium , biochemistry , fluoride , biology , inorganic chemistry , organic chemistry
We have reported recently that prostaglandin E 2 (PGE 2 ) stimulated phosphoinositide metabolism in bovine adrenal chromaffin cells and that PGE 2 and ouabain, an inhibitor of Na + ,K + ‐ATPase, synergistically induced a gradual secretion of catecholamines from the cells. Here we examined the involvement of a GTP‐binding protein(s) in PGE receptor‐induced responses by using NaF. In the presence of Ca 2+ in the medium, NaF stimulated the formation of all three inositol phosphates, i.e., inositol monophosphate, bisphosphate, and trisphosphate, linearly over 30 min in a dose‐dependent manner (15–30 m M ). This effect on phosphoinositide metabolism was accompanied by an increase in cytosolic free Ca 2+ . NaF also induced catecholamine release from chromaffin cells, and the dependency of stimulation of the release on NaF concentration was well correlated with those of NaF‐enhanced inositol phosphate formation and increase in cytosolic free Ca 2+ . Although the effect of NaF on PGE 2 ‐induced catecholamine release in the presence of ouabain was additive at concentrations below 20 m M , there was no additive effect at 25 m M NaF. Furthermore, the time course of catecholamine release stimulated by 20 m M NaF in the presence of ouabain was quite similar to that by 1 μ M PGE 2 , and both stimulations were markedly inhibited by amiloride, with half‐maximal inhibition at 10 μ M. Pretreatment of the cells with pertussis toxin did not prevent, but rather enhanced, PGE 2 ‐induced catecholamine release over the range of concentrations examined. These results demonstrate that NaF mimics the effect of PGE 2 on catecholamine release from chromaffin cells and suggest that PGE 2 ‐evoked catecholamine release may be mediated by the stimulation of phosphoinositide metabolism through a putative GTP‐binding protein insensitive to pertussis toxin.