
<ArticleTitle><prot>beta(1)-Adrenoceptor</prot> antibodies induce positive inotropic response in isolated cardiomyocytes.</ArticleTitle>
<AbstractText><prot>beta(1)-Adrenoceptor</prot> autoantibodies are present in approximately 30% of patients suffering from dilated cardiomyopathy. The inotropic effects mediated by these antibodies remain to be studied. Monoclonal antibodies were raised against a peptide corresponding to the second extracellular loop of the human <prot>beta(1)-adrenoceptor</prot> in balb/C mouse (n=6), and were characterized by enzyme immunoassay after purification by protein A. Purified immunoglobulin G from non-immunized animals (controls) did not influence Ca(2+) transient and cell shortening of rat cardiomyocytes measured by confocal-laser-scanning-microscopy. <prot>beta(1)-adrenoceptor</prot> antibodies caused a dose-related increase in Ca(2+) transient (dilution 1:2: +35.3+/-5.1%), and in cell shortening (dilution 1:2: +40.5+/-6.3%) (P&#60;0.01 vs. controls). The effect of the <prot>beta(1)-adrenoceptor</prot> antibodies was blocked by the antigenic peptide and by the antagonist metoprolol. In addition, <prot>beta(1)-adrenoceptor</prot> antibodies induced a dose-dependent increase of the cyclic adenosine monophosphate. The inotropic response induced by isoproterenol was attenuated by the <prot>beta(1)-adrenoceptor</prot> antibody. <prot>beta(1)-adrenoceptor</prot> antibodies as partial agonists induce a specific positive inotropic effect via the <prot>protein-kinase-A</prot>-cascade.</AbstractText>
