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.