| Abstract: | ![]()
Adrenergic receptors mediating depolarization in in vitro neonatal rat brown adipose tissue (BAT) have been characterized by use of adrenergic agonists and antagonists. Releasable endogenous catecholamine was present in BAT as demonstrated by tyramine- and 1,1-dimethyl-4-phenylpiperazinium iodide- (DMPP) induced depolarization in BAT from normal rats and its absence when BAT from reserpinized rats was used. In BAT from reserpinized rats l-norepinephrine, l-phenylephrine, and l-isoproterenol all similarly depolarized the bronw adipocytes over the concentration range of 10(-8) to 10(-6) M with a maximal depolarization of about 25 mV. Dopamine and d-norepinephrine were more than 100 times less potent. The beta-adrenergic blocker propranolol competitively inhibited isoproterenol-induced depolarization, whereas the alpha-adrenergic blackers, phentolamine and phenoxybenzamine, inhibited the phenylephrine-induced depolarization with much smaller inhibitory effects on the isoproterenol-induced depolarization. Both phenylephrine and isoproterenol elicited transient depolarizations when briefly added to the bathing medium while continuously recording from the same cell. Both the agonist and antagonist studies are interpreted as indicating the presence of both alpha- and beta-adrenergic receptors on BAT cells which mediate catecholamine-induced depolarization. |
