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Relative contribution of the Na + /Ca 2+ exchanger, mitochondria and endoplasmic reticulum in the regulation of cytosolic Ca 2+ and catecholamine secretion of bovine adrenal chromaffin cells
Author(s) -
Yang DeMing,
Kao LungSen
Publication year - 2001
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 - 10.1046/j.1471-4159.2001.00055.x
Subject(s) - endoplasmic reticulum , cytosol , secretion , chromaffin cell , chemistry , calcium , fura 2 , exocytosis , medicine , catecholamine , mitochondrion , endocrinology , biophysics , adrenal medulla , biology , biochemistry , enzyme , organic chemistry
The relative importance of mitochondria, the Na + /Ca 2+ exchanger (NCX) and the endoplasmic reticulum (ER) in the regulation of the cytosolic Ca 2+ concentration ([Ca 2+ ] i ) were examined in bovine chromaffin cells using fura‐2 for average [Ca 2+ ] i and amperometry for secretory activity, which reflects the local Ca 2+ concentration near the exocytotic sites. Chromaffin cells were stimulated by a high concentration of K + when the three Ca 2+ removal mechanisms were individually or simultaneously inhibited. When the mitochondrial Ca 2+ uptake was inhibited, the [Ca 2+ ] i decayed at a significantly slower rate and the secretory activity was higher than the control cells. The NCX appears to function only in the initial phase of [Ca 2+ ] i decay and when the ER Ca 2+ pump is blocked. Similarly, the ER had a significant effect on the [Ca 2+ ] i decay and on the secretion only when the NCX was blocked. Inhibition of all three mechanisms leads to a substantial delay in [Ca 2+ ] i recovery and an increase in the secretion. The results suggest that the three mechanisms work together in the regulation of the Ca 2+ near the Ca 2+ channels and exocytotic sites and therefore modulate the secretory activity. When Ca 2+ diffuses away from the exocytotic sites, the mitochondrial Ca 2+ uptake becomes the dominant mechanism.