[Interaction of antibodies with cardiac neurotransmitter receptors].

This paper demonstrates that antibodies against neurotransmitter receptors of the cardiac membrane are able to alter the physiology, pharmacology and biochemistry of the target organ. Sera from chagasic patients contain an antibody which binds to beta adrenoceptors of myocardium and modulates their activity. Chagasic IgG simulates a partial beta agonist by increasing contractility and diminishing reactivity to exogenous norepinephrine. Moreover, chagasic IgG inhibits the binding of the specific radioligand to purified cardiac membranes. The interaction of chagasic IgG with beta-adrenoceptors triggers signal transduction resulting in the stimulation of adenylate cyclase with an increased production of cAMP. Stimulation of Ca(++)-ATPase and inhibition of Na+ + K(+)-ATPase are also observed. These enzyme dysfunctions induce modifications of cellular thermodynamic equilibrium that trigger both morphological and functional alterations of the myocardium. Other immune sera can also trigger pharmacologic effects on isolated atria. Immune IgG directed against specific alloantigens and IgG from mice with autoimmune myocarditis are able to recognize the beta adrenergic receptor-coupled adenylate cyclase system and alter the function of target organs. The detection of antibodies against neurotransmitter receptors could be a useful marker during the early stages of development of autoimmune diseases.