Alpha and beta-adrenergic mediation of membrane potential changes and metabolism in rat brown adipose tissue.

Membrane potential and flavoprotein redox state have been measured simultaneously and continuously in brown adipose tissue in order to determine how nerve stimulation and adrenergic agonists control its metabolic activity. Both trains of nerve impulses and addition of noradrenaline evoke two temporally distinct cell depolarizations. The first rapid depolarization precedes the increase in flavoprotein reduction. With nerve stimulation, at the time of maximum flavoprotein reduction the cell has repolarized or hyperpolarized. The second slow depolarization follows flavoprotein reduction. Phentolamine, an alpha antagonist, selectively blocks the first depolarization, but not the flavoprotein reduction. However the time of maximum flavoprotein reduction is delayed. Propranolol, a beta antagonist, delays the first repolarization until the end of nerve stimulation and inhibits the transient hyperpolarization, second depolarization and flavoprotein reduction. Isoproterenol, a beta agonist, or the fatty acid octanoate produce only a transient hyperpolarization and subsequent slow depolarization following flavoprotein reduction. Thus brown adipose tissue contains both alpha- and beta-adrenergic receptors. Stimulation of alpha receptors produces an early membrane depolarization. Stimulation of beta receptors leads to an increase in metabolic activity which then appears to produce slow changes in membrane potential.