Treatment with β1-selective antagonists causes selective sensitization of isolated strips of human atrial myocardium to the inotropic action of epinephrine and β2-agonists but not of norepinephrine. To determine whether β1-selective antagonist treatment alters the responsiveness of cardiac β2-adrenoreceptors in vivo, we measured the positive chronotropic responses to salbutamol injected into the right coronary artery. Ten patients treated with atenolol (50-100 mg daily) were compared with 10 patients not treated with β-blockers. The mean dose required to cause an increase in heart rate of 30 beats/min was 2.29 μg (log dose 0.36±0.12 μg [mean±SEM]) in the atenolol-treated patients. In the non-β-blocker-treated patients, the dose required to cause an increase in heart rate of 30 beats/min was significantly greater, 8.91 μg (log dose 0.95±0.11 μg) (p<0.005). We conclude that treatment with β1-selective β-blockers leads to increased cardiac responsiveness to β2-adrenoreceptor stimulation. This may be the underlying mechanism of the β-blocker withdrawal syndrome and may make the heart more susceptible to the adverse effects of epinephrine in situations of stress (e.g., myocardial infarction).
CITATION STYLE
Hall, J. A., Petch, M. C., & Brown, M. J. (1991). In vivo demonstration of cardiac β2-adrenoreceptor sensitization by β1-antagonist treatment. Circulation Research, 69(4), 959–964. https://doi.org/10.1161/01.RES.69.4.959
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