Central hemodynamic effects of adrenaline with special reference to β2‐adrenergic influence on heart rate and cardiac afterload in anesthetized cats

Central hemodynamic responses evoked by i. v.infusions of adrenaline and noradrenaline were studied in normovolemic anesthetized cats with intact adrenoceptors, after selective β2-blockade (ICI 118,551), and after nonselective β-blockade (propranolol).The results demonstrated the presence of an important β2-adrenergic component in the integrated response to ‘physiological’ doses of adrenaline contributing to increased cardiac output, decreased total peripheral resistance and virtually unchanged mean arterial blood pressure. Corresponding β2-adrenergic effects of noradrenaline were small. The β2-adrenergic effects of adrenaline on the heart seemed to be both direct and indirect. A moderate direct chronotropic response mediated by β2-adrenoceptors apparently was present but there was no evidence of a direct β2-adrenergic inotropic effect. An indirect, quite marked effect on the heart was accomplished by a β2-adrenergic vasodilator interaction with the α-adrenergic vasoconstrictor influence on the systemic resistance vessels. This caused a net decrease in total peripheral resistance, thereby preventing an undue increase in cardiac afterload (arterial pressure) which seemed to be essential for evoking ‘optimal’ increases in cardiac output. It is suggested that such adrenaline evoked indirect, β2-adrenergic improvement of cardiac performance is of functional importance in reflex sympatho-adrenal circulatory control.