Autoantibodies to the 𝜷_𝟏-Adrenoceptor from Patients with Periodontitis as a Risk Factor for Cardiac Dysfunction

Table 3

Influence of β ₁ blockade on the stimulatory and inhibitory effects of anti-β ₁-AR peptide IgG.

Addition	dF/dt	cAMP	cGMP
Basal	1.8 ± 0.21	0.38 ± 0.03	0.041 ± 0.004
β 1-AR IgG (5×10^−8 M)	3.9 ± 0.32*	1.25 ± 0.11*	0.051 ± 0.004
β 1-AR IgG (5×10^−8 M) + atenolol	2.1 ± 0.19**	0.41 ± 0.04**	—
β 1-AR IgG + β 1-AR peptide	2.3 ± 0.23**	0.42 ± 0.03**	—
Normal IgG (5×10^−8 M)	1.9 ± 0.18	0.40 ± 0.02	0.039 ± 0.04
Basal	2.1 ± 0.22	0.40 ± 0.03	0.042 ± 0.004
β 1-AR IgG (5×10^−7 M)	0.6 ± 0.05*	0.21 ± 0.02*	0.350 ± 0.03*
β 1-AR IgG (5×10^−7 M) + atenolol	1.7 ± 0.15**	0.38 ± 0.03**	0.122 ± 0.02**
β 1-AR IgG + β 1-AR peptide	1.9 ± 0.20**	0.37 ± 0.02**	0.101 ± 0.02**
Normal IgG (5×10^−7 M)	2.0 ± 0.19	0.42 ± 0.03	0.043 ± 0.003

Values are mean ± s.e.m. of ten patients with periodontitis in each group carried out in duplicate. Contractility (dF/dt: g/s), and levels of cAMP (pmol/mg tissue ww) and cGMP (pmol/mg tissue ww) were measured after incubation for 15 min with rat atria in the presence of anti-β ₁-AR peptide IgG (β ₁-AR IgG) and normal IgG or in the absence (basal) of IgG. Atenolol (5×10⁻⁷ M) and β ₁-AR peptide (5×10⁻⁵ M) were added before the IgG. *𝑃<0.001 versus basal; **𝑃<0.001 versus β ₁-AR IgG alone.