[Adrenergic betareceptors and cardiac insufficiency]

Noradrenergic sympathetic tone is always increased in chronic left ventricular failure of which it is one of the main compensatory mechanisms. Beta-1-adrenergic stimulation increases the heart rate and left ventricular contractility. However, the efficacy of this "compensatory" mechanism is limited on the one hand by the energetic cost of inotropic stimulation and, on the other hand, by the phenomenon of desensitisation and down-regulation of myocardial beta-1-receptors during intense and prolonged noradrenergic stimulation as observed in chronic cardiac failure. These physiopathological concepts raise the question of the indications of drugs affecting betareceptors in cardiac failure. Positive inotropic beta-mimetics can only be used during short periods of acute decompensation: low dose betablocker therapy protects the betareceptors from the phenomenon of desensitisation and seem to exert a beneficial action in this way in some cases of cardiac failure; these preliminary results require confirmation by large scale controlled therapeutic trials. Finally, a new pharmacological class of drugs, the beta-1 adrenergic partial agonists, seems to be useful in the management of moderate degrees of cardiac failure due to ischemic heart disease.