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 beta 2-blockade (ICI 118,551), and after nonselective beta-blockade propranolol). The results demonstrated the presence of an important beta 2-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 beta 2-adrenergic effects of noradrenaline were small. The beta 2-adrenergic effects of adrenaline on the heart seemed to be both direct and indirect. A moderate direct chronotropic response mediated by beta 2-adrenoceptors apparently was present but there was no evidence of a direct beta 2-adrenergic inotropic effect. An indirect, quite marked effect on the heart was accomplished by a beta 2-adrenergic vasodilator interaction with the alpha-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, beta 2-adrenergic improvement of cardiac performance is of functional importance in reflex sympatho-adrenal circulatory control.