, Volume 348, Issue 5, pp 536-540

Both β1- and β2-adrenoceptors mediate catecholamine-evoked arrhythmias in isolated human right atrium

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Summary

The involvement of β1- and β2-adrenoceptors in catecholamine-evoked arrhythmias was investigated in isolated human right atrial appendages obtained from 22 patients chronically treated with β blockers (usually β1-selective) and 9 patients not treated with β blockers. A simple experimental model that assesses the incidence of arrhythmic contractions as a function of heart rate (pacing) is introduced. β1-adrenoceptors were activated by (−)-noradrenaline during β2-adrenoceptor blockade with 50 nmol/l ICI 118551. β2-adrenoceptors were activated by (−)-adrenaline during β1-adrenoceptor blockade with 300 nmol/l CGP 20712A. Both (−)noradrenaline and (−)-adrenaline caused arrhythmic contractions whose incidence was greater at low than at high pacing rates. CGP 20712A (300 nmol/l) blocked the (−)-noradrenaline-evoked contractions in 1/1 atrial strip from 1/1 patient not treated with a β blocker and 17/17 atrial strips from 15/15 patients chronically treated with β blockers. ICI 118551 (50 nmol/l) blocked the (−)-adrenaline-evoked contractions in 3/4 atrial strips from 3/4 patients not treated with β blockers and 17/20 atrial strips from 15/18 patients chronically treated with β blockers. The incidence of arrhythmic contractions evoked by both (−)-noradrenaline and (−)-adrenaline was higher in chronically β blocked patients than in non β blocked patients. We conclude that both β1- and β2-adrenoceptors mediate atrial arrhythmias and that the generation of these arrhythmias is facilitated by chronic β1-adrenoceptor blockade.

Correspondence to: A. J. Kaumann at the Clinical Pharmacology Unit, University of Cambridge, as above