Antilaminin IgG triggers the murine atria phosphoinositide hydrolysis through muscarinic receptor stimulation

Hearts from mice hyperimmunized with cardiac tissue were studied to evaluate the expression and biological activity of muscarinic cholinergic receptors and immunoglobulin G deposits along the immunization period. Mice were sacrificed at 10 day intervals from the first injection up to day 100. Simultaneously, the activity of autoantibodies against muscarinic receptors on normal hearts was also examined in sera. Hearts with autoimmune myocarditis showed a muscarinic receptor-related dysfunction, with an impaired response to exogenous muscarinic agonists and a significant reduction in muscarinic binding sites, both effects being maximum at 40-50 days post-immunization. In addition, serum or immunoglobulin G from mice with myocarditis were able to interact with muscarinic acetylcholine receptors displaying a partial agonist effect. Autoimmune sera and immunoglobulin G reduced heart contractility while inhibited 3H-QNB binding to cardiac acetylcholine receptors in a concentration dependent manner showing the highest effects at days 40-50 and decreased progressively thereafter. The development of muscarinic receptor-related cardiac dysfunction may be associated with the presence of circulating antibodies having muscarinic receptor activity. These studies are of relevance to clinical conditions such as Chagas' disease, where immunological processes involving the cholinergic system are considered to cause cardiomyopathy.

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Alterations in cardiac muscarinic acetylcholine receptors in mice with autoimmune myocarditis and association with circulating muscarinic receptor-related autoantibodies

Leirós

Goren

Sterin‐Borda

et al. 1994

Clinical Autonomic Research

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Pharmacological evidence for the existance of different subtypes of muscarinic acetylcholine receptors for phosphoinositide hydrolysis in neonatal versus adult rat atria

JoséCamusso

Sterin‐Borda

Rodríguez

et al. 1995

Journal of Lipid Mediators and Cell Signalling

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Cardiac beta-receptors in experimental Chagas' disease

Enders

Paglini

Fernández

et al. 1995

Rev. Inst. Med. trop. S. Paulo

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Experimental Chagas' disease (45 to 90 days post-infection) showed serious cardiac alterations in the contractility and in the pharmacological response to beta adrenergic receptors in normal and T. cruzi infected mice (post-acute phase). Chagasic infection did not change the beta receptors density (78.591 +/- 3.125 fmol/mg protein and 73.647 +/- 2.194 fmol/mg protein for controls) but their affinity was significantly diminished (Kd = 7.299 +/- 0.426 significantly diminished (Kd = 7.299 +/- 0.426 nM and Kd = 3.759 +/- 0.212 nM for the control) p < 0.001. This results demonstrate that the alterations in pharmacological response previously reported in chagasic myocardium are related to a significantly less beta cardiac receptor affinity. During this experimental period serious cardiac cell alterations take place and functional consequences will be detected in the chronic phase.

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Antilaminin IgG triggers the murine atria phosphoinositide hydrolysis through muscarinic receptor stimulation

Cited by 3 publications

References 14 publications

Alterations in cardiac muscarinic acetylcholine receptors in mice with autoimmune myocarditis and association with circulating muscarinic receptor-related autoantibodies

Alterations in cardiac muscarinic acetylcholine receptors in mice with autoimmune myocarditis and association with circulating muscarinic receptor-related autoantibodies

Pharmacological evidence for the existance of different subtypes of muscarinic acetylcholine receptors for phosphoinositide hydrolysis in neonatal versus adult rat atria

Cardiac beta-receptors in experimental Chagas' disease

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