α 1-Adrenergic stimulation of Cl − efflux in isolated brown adipocytes

Unidirectional 36Cl − efflux from preloaded isolated brown adipocytes was studied. A norepinephrine-stimulated 36Cl − efflux pathway was found which approximately doubled the rate of 36Cl − efflux from the cells. The response to norepinephrine was fully inhibited by the α 1-adrenergic antagonist pra...

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Bibliographic Details
Published in:FEBS letters 1990-03, Vol.262 (1), p.25-28
Main Authors: Dasso, Leonardo, Connolly, Eamonn, Nedergaard, Jan
Format: Article
Language:English
Subjects:
Adipose Tissue, Brown - metabolism
Animals
Brown adipose tissue
Calcium - physiology
Chlorides - metabolism
Cl − flux
Cricetinae
Hamster
In Vitro Techniques
Membrane depolarization
Membrane Potentials
Mesocricetus
Nonshivering thermogenesis
Norepinephrine - pharmacology
Prazosin
Receptors, Adrenergic, alpha - physiology
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Summary:Unidirectional 36Cl − efflux from preloaded isolated brown adipocytes was studied. A norepinephrine-stimulated 36Cl − efflux pathway was found which approximately doubled the rate of 36Cl − efflux from the cells. The response to norepinephrine was fully inhibited by the α 1-adrenergic antagonist prazosin, but was unaffected by the β-adrenergic antagonist propranolol, showing that norepinephrine stimulated the 36Cl − efflux pathway via the α 1-adrenoceptor. The stimulation of 36Cl − efflux could not be mimicked by the Ca 2+ ionophore A23187, indicating that the effect was not mediated by elevation of the intracellular Ca 2+ level. It is concluded that brown fat cells possess a specific mechanism for α 1-adrenergic stimulation of Cl − efflux. The possibility is discussed that this Cl − efflux pathway could be the basis for the early α-adrenergic depolarization seen in brown fat cells.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(90)80144-8