Labetolol, which blocks both alpha and beta-adrenoceptors, was found to have direct actions on cardiac muscle which could themselves be antiarrhythmic. It depressed the maximum rate of depolarisation, and reduced conduction velocity, in atrial and ventricular muscle and in Purkinje cells, implying restriction of fast inward current (Class 1). It had twice the potency of procaine as a local anesthetic on nerve. Labetolol abbreviated the action potential (AP) plateau in normoxic atrial muscle, but attenuated AP-shortening by hypoxia. It caused a significant slowing of all phases of repolarisation (Class 3) in normoxic ventricular muscle. It had no negative inotropic action in normoxia or hypoxia, and there was no evidence for slowing of A-V nodal conduction.
