PGE2 and 6-keto-PGF1alfa generation and cyclic AMP in the atria of rats during normoxia and hypoxia

Abstract

Circulating antibodies can be detected in chronic periodontitis patients given the presence of serum auto antibodies against β1-adrenoceptor (β1-AR) in periodontitis patients by using cardiac membranes or a synthetic β1-AR peptide corresponding to the second extracellular loop of human β1-AR as antigens. Periodontitis patients also exhibit enhanced atria contractility in normoxia and tonic contraction in hypoxia. Atenolol, synthetic β1 peptide and nifedipine abrogate the action of both Isoproterenol and β1 IgG on atria contractility in both experimental conditions. In turn, β1 IgG display a partial agonist-like activity and modifies the contractility of isolated atria, accompanied by an accumulation of cyclic AMP nucleotide in normoxia and hypoxia. The autoantibody is able to provoke an increment in the concentrations of PGE2 and 6-keto-PGF1α, which is abrogated by preincubating atria with adrenergic antagonist, synthetic β1 peptide and prostanoid receptor antagonists. On this basis this study seeks to correlate the periodontitis infection to an increased risk of cardiac disease high lightening the role of β1 IgG in the alteration of myocardial contractility and the subsequent increment of prostaglandins (PGE2 and 6-keto-PGF1α,) accompanied by an increment in the production of cyclic AMP, resulting in an effective adaptation of myocardium function in acute ischemia.