International Scholarly Research Notices / 2011 / Article / Tab 3

Research Article

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.

AdditiondF/dtcAMPcGMP

Basal1.8 ± 0.210.38 ± 0.030.041 ± 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) + atenolol2.1 ± 0.19**0.41 ± 0.04**
β 1-AR IgG + β 1-AR peptide2.3 ± 0.23**0.42 ± 0.03**
Normal IgG (5 × 10−8 M)1.9 ± 0.180.40 ± 0.020.039 ± 0.04

Basal2.1 ± 0.220.40 ± 0.030.042 ± 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) + atenolol1.7 ± 0.15**0.38 ± 0.03**0.122 ± 0.02**
β 1-AR IgG + β 1-AR peptide1.9 ± 0.20**0.37 ± 0.02**0.101 ± 0.02**
Normal IgG (5 × 10−7 M)2.0 ± 0.190.42 ± 0.030.043 ± 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 . 0 0 1 versus basal; ** 𝑃 < 0 . 0 0 1 versus β 1-AR IgG alone.

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