Alpha 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 alpha 1-adrenergic antagonist prazosin, but was unaffected by the beta-adrenergic antagonist propranolol, showing that norepinephrine stimulated the 36Cl- efflux pathway via the alpha 1-adrenoceptor. The stimulation of 36Cl- efflux could not be mimicked by the Ca2+ ionophore A23187, indicating that the effect was not mediated by elevation of the intracellular Ca2+ level. It is concluded that brown fat cells possess a specific mechanism for alpha 1-adrenergic stimulation of Cl- efflux. The possibility is discussed that this Cl- efflux pathway could be the basis for the early alpha-adrenergic depolarization seen in brown fat cells.
Dasso
L
L
Wenner-Gren Institute, University of Stockholm, Arrhenius Laboratories F3, Sweden.
Connolly
E
E
Nedergaard
J
J
D002001:Adipose Tissue, Brown / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000502:physiology; D002712:Chlorides / Q000378:metabolism*; D006224:Cricetinae; D066298:In Vitro Techniques; D008564:Membrane Potentials; D008647:Mesocricetus; D009638:Norepinephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D002712:Chlorides; D011942:Receptors, Adrenergic, alpha; D002118:Calcium; D009638:Norepinephrine