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 α1-adrenergic antagonist prazosin, but was unaffected by the β-adrenergic antagonist propranolol, showing that norepinephrine stimulated the 36Cl− efflux pathway via the α1-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 α1-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.
