Selective inhibition of cholera toxin and catecholamine stimulated lipolysis by blocking agents

M. S. Katz, W. B. Greenough

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)964-968
Number of pages5
JournalInfection and immunity
Volume12
Issue number5
DOIs
StatePublished - 1975

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

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