Vibrio cholerae enterotoxin stimulates lipolysis in rat epididymal fat cell suspensions. Like hormones this toxin increases adenylate cyclase activity, raising levels of cyclic adenosine 3',5' monophosphate (cAMP), which activates a cellular lipase. Using specific blocking agents, we studied the responses to the adrenergic lipolytic hormones epinephrine, norepinephrine, and isoproterenol, and to cholera toxin. All stimulators were used at 100 x threshold dose. Propranolol (34 μM), a β blocking agent, inhibited epinephrine stimulation (P<0.001) but not that of toxin (P>0.2). Choleragenoid (25 μg/ml), a natural toxoid of cholera toxin, blocked stimulation by toxin (P<0.001) but not that of the adrenergic agents (P>0.2). A β blocker, practolol (3 mM), inhibited stimulation by the catecholamines tested (P<0.005) but not that of toxin (P>0.05). Higher concentrations of propranolol (340 μM) and the α blocking agents phenoxybenzamine (3 mM) and phentolamine (1.6 mM) inhibited all agonists (P<0.001). The response to theophylline was inhibited by all blockers (P<0.05) except propranolol at the lower concentration (34 μM). A combined β and α blockade using propranolol and epinephrine together did not inhibit toxin mediated lipolysis. It appears that stimulation by cholera toxin is independent of β adrenergic receptors. A major inhibition of theophylline mediated lipolysis by α blocking drugs indicated a nonspecific effect of these agents at the concentrations used. The uninhibited response to toxin in the presence of propranolol and epinephrine suggests a lack of relationship of the toxin receptor to either α or β receptors.
ASJC Scopus subject areas
- Infectious Diseases