Key result
Autoimmune IgG impairs cardiac contractility by simulating cholinergic agonists at myocardial muscarinic receptors.
Why the study?
The role of muscarinic cholinergic receptor-binding components in IgG from experimental autoimmune myocarditis and their effect on cardiac function was investigated.
Answers are grounded in this paper and cite their sources.
May support autoantibody effects on cardiac muscarinic signaling in myocarditis models; leaves open relevance to human disease.
Evidence is presented showing that in experimental autoimmune myocarditis, there are certain components in IgG fraction of the sera that bind to myocardium muscarinic cholinergic receptors. The autoimmune IgG simulated the biologic effect of cholinergic agonists because (i) it increased cGMP levels, (ii) it decreased cAMP stimulated levels, and (iii) it reduced heart contractility and diminished reactivity to exogenous acetylcholine. Autoimmune IgG inhibited the binding of specific muscarinic cholinergic radioligand to purified myocardial membranes behaving as noncompetitive inhibitors. The recognition appears to be organ specific because the autoimmune IgG did not bind to muscarinic cholinergic receptors of urinary bladder. The presence of antibodies against antigens expressed in an accessible form to antibody in living myocardial cells might be related to some of the immunopathologic mechanisms participating in the pathogenesis of the experimental autoimmune myocarditis.
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Leirós et al. (1990) studied Experimental autoimmune myocarditis. Autoimmune IgG was evaluated on Muscarinic cholinergic receptor binding and cardiac contractility. Autoimmune IgG in experimental autoimmune myocarditis bound to myocardial muscarinic cholinergic receptors, simulating cholinergic agonists and reducing heart contractility.
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