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Caffeine‐Sensitive Calcium Stores in Bovine Adrenal Chromaffin Cells
Author(s) -
Liu PeiShan,
Lin YiJen,
Kao LungSen
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.tb02577.x
Subject(s) - caffeine , extracellular , ionomycin , chromaffin cell , calcium , chemistry , intracellular , fura 2 , inositol , endocrinology , medicine , inositol trisphosphate , cytosol , biochemistry , biology , adrenal medulla , catecholamine , receptor , enzyme , organic chemistry
Caffeine was used to study the intracellular Ca 2+ pools of bovine chromaffin cells. Its effects on cytosolic Ca 2+ concentration ([Ca 2+ ] i ) were examined using fura‐2. Caffeine caused a transient increase in [Ca 2+ ] i in the presence or absence of extracellular Ca 2+ . In the former case, the caffeineinduced [Ca 2+ ] i increase was higher and stayed above the basal value for several minutes. In the latter case, the [Ca 2+ ] i rise was lower and fell to the basal level within 1 min. These results suggest that caffeine increases [Ca 2+ ] i by causing both Ca 2+ influx and Ca 2+ release from intracellular pools. In the absence of extracellular Ca 2+ , ionomycin but not caffeine caused a further increase in [Ca 2+ ] i in cells that had been treated with caffeine. Apparently there are at least two intracellular Ca 2+ pools, only one of which is sensitive to caffeine. The caffeine‐induced [Ca 2+ ] i rise became smaller when the cells were pretreated with the inositol trisphosphate‐generating agonists, methacholine and bradykinin. In addition, metha‐choline was unable to initiate a [Ca 2+ ] i transient after the cells had been treated with caffeine. The results indicate that the caffeine‐sensitive Ca 2+ pools overlap with the inositol trisphosphate‐sensitive pool and that the size, of the latter pool is smaller than that of the former. The caffeine‐sensitive Ca 2+ pools were refilled after high K+ treatment, which suggests that the caffeine‐sensitive Ca 2+ pools may be important in buffering the cytosolic Ca 2+ . The effect of caffeine on [Ca 2+ ] i is not due to inhibition of phosphodiesterase. Our results support a Ca 2+ entry model in which depletion of intracellular Ca 2+ pools controls the rate of Ca 2+ entry across the plasma membrane.