The human heart contains both β1-adrenoceptors and a considerable number of β2-adrenoceptors, both of which bring about positive inotropic and chronotropic effects of β-adrenoccptor agonists in vitro and in vivo. In chronic heart failure, the decrease in β-adrenoceptor function is related to the severity of the disease. However, both cardiac β1,- and β2-adrenoccptors seem to be differentially affected depending on the type of heart failure and its aetiology. β1-adrenoceptor function decreases in all forms of chronic heart failure. β2-adrenoceptor function, on the other hand, decreases in mitral valve disease, tetralogy of Fallot and end-stage ischaemic cardiomyopathy, and seems to be unaltered (or only mildly uncoupled) in end-stage dilated cardiomyopathy, and possibly in aortic valve disease. Since the human heart has few spare β-adrenoccptors and these decline with increasing degree of heart failure, β-adrenoceptor agonists (but only non-selective full agonists) may be of therapeutic use only if the heart needs acute inotropic support; in long-term treatment they may be not effective, since tolerance develops. On the other hand, for long-term treatment selective β1,-adrenoccptor antagonists may be beneficial since they protect the heart from the deleterious effects of chronic exposure to high (cardiac derived) noradrenaline and simultaneously may restore the previously reduced fi-adrenoceptor function.

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