Alpha- and beta-adrenergic mediation of changes in metabolism and Na/K exchange in rat brown fat.

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Abstract
Double- and triple-barreled ion-sensitive microelectrodes were used to measure changes in extracellular K+ and Na+ concentrations ([K+]o, [Na+]o) in brown fat. Redox states of different respiratory enzymes were measured simultaneously in order to correlate ion movements with metabolic activity. Trains of stimuli applied to the efferent nerves evoked two distinct increases in [K+]o. A first, small, rapid increase occurred within 10 s and accompanied a first, rapid membrane depolarization. A second, slow increase of [K+]o occurred several minutes after stimulation and accompanied a second, slow depolarization. A few seconds after stimulation onset, while the membrane was repolarizing and shifts in redox states indicated increases in lipolysis and respiration, [K+]o decreased. The [K+]o decrease was accompanied by an increase in [Na+]o, and could be partly blocked by ouabain. Phentolamine, an alpha-antagonist that blocks the first depolarization, also blocked the first, rapid [K+]o increase and part of the subsequent decrease. Propranolol, a beta-antagonist, had little effect on the first depolarization and the first increase in [K+]o, but blocked part of the subsequent [K+]o decrease and the second, slow [K+]o increase. The changes in [K+]o were almost completely abolished in the presence of both antagonists. It is concluded that brown adipocytes take up K+ and simultaneously lose Na+ in response to the interaction of noradrenaline with alpha- and beta-receptors, and this indicates a very early stimulation of the Na+ pump.