Endotoxicosis decreases beta-adrenergic receptor-mediated stimulation of myocardial adenylate cyclase during the agonal stage without inhibiting the enzyme system itself.
Agonal-stage beta-adrenergic desensitization in endotoxic rats without cyclase inhibition; leaves open relevance to human septic cardiomyopathy.
The effect of in vivo endotoxin administration on adenylate cyclase in rat ventricular membranes was studied. Basal, fluoride-, and 5'-guanylylimidodiphosphate-stimulated adenylate cyclase activities were not affected throughout the period of endotoxicosis. Isoproterenol-stimulated adenylate cyclase activity was not different at 0.5 or 3 h after endotoxin. At the agonal stage, the isoproterenol dose-response curve was shifted significantly to the right in myocardial membranes from endotoxic rats, but there was no significant decrease in maximum stimulated activity. These data indicate that endotoxicosis does not inhibit the adenylate cyclase enzyme system but does decrease stimulation of adenylate cyclase via beta-adrenergic receptors when the animal is approaching death.
No takes yet. Share an insight, caveat, or question.
Romano et al. (1986) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: