Beta-adrenergic potentiation of endoplasmic reticulum Ca(2+) release in brown fat cells

We find that the adrenergic agonist isoproterenol increases intracellular Ca(2+) concentration ([Ca(2+)](i)) in cultured rat brown adipocytes. At the concentration used (10 microM), isoproterenol-induced Ca(2+) responses were sensitive to block by either alpha(1)- or beta-adrenergic antagonists, sug...

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Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology 2002-05, Vol.282 (5), p.C1016-C1024
Main Authors: Leaver, Eric V, Pappone, Pamela A
Format: Article
Language:English
Subjects:
Adipocytes - cytology
Adipocytes - drug effects
Adipocytes - metabolism
Adipose Tissue, Brown - cytology
Adipose Tissue, Brown - drug effects
Adipose Tissue, Brown - metabolism
Adrenergic Agonists - pharmacology
Adrenergic alpha-Antagonists - pharmacology
Adrenergic beta-Agonists - pharmacology
Adrenergic beta-Antagonists - pharmacology
Animals
Calcium - metabolism
Cells, Cultured
Endoplasmic Reticulum - metabolism
Enzyme Inhibitors - pharmacology
Ethanolamines - pharmacology
Isoproterenol - pharmacology
Prazosin - pharmacology
Propranolol - pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Purinergic P2 - metabolism
Thapsigargin - pharmacology
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Summary:We find that the adrenergic agonist isoproterenol increases intracellular Ca(2+) concentration ([Ca(2+)](i)) in cultured rat brown adipocytes. At the concentration used (10 microM), isoproterenol-induced Ca(2+) responses were sensitive to block by either alpha(1)- or beta-adrenergic antagonists, suggesting an interaction between these receptor subtypes. Despite reliance on beta-adrenoceptor activation, the Ca(2+) response was not due solely to increases in cAMP because, administered alone, the selective beta(3)-adrenergic agonist BRL-37344 or forskolin did not increase [Ca(2+)](i). However, increased cAMP elicited vigorous [Ca(2+)](i) increases in the presence of barely active concentrations of the alpha-adrenergic agonist phenylephrine or the P2Y receptor agonist UTP. Consistent with isoproterenol recruiting only inositol 1,4,5-trisphosphate (IP(3))-sensitive Ca(2+) stores, endoplasmic reticulum store depletion by thapsigargin blocked isoproterenol-induced Ca(2+) increases, but removal of external Ca(2+) did not. These results argue that increases in cAMP sensitize the IP(3)-mediated Ca(2+) release system in brown adipocytes.
ISSN:0363-6143
DOI:10.1152/ajpcell.00204.2001