Cardiac effects of secretin; an approach to its mechanisms of action as shown by beta-adrenergic blockade and measurement of left ventricular dimensions in dogs.

In previous studies, the peptide secretin has demonstrated the ability to increase cardiac output and peripheral organ flow. In this investigation the mechanisms of the myocardial effects of secretin were studied. The secretin effects on cardiac output, stroke volume and systemic resistance were unaltered after propranolol, whereas the effect on LVdP/dt was reduced and the heart rate effect negligible. Systemic pressure, myocardial blood flow and myocardial oxygen consumption were unchanged by secretin infusion both before and after beta-receptor blockade. Secretin caused reduction of all three end-systolic left ventricular diameters. Thus, an inotropic effect by secretin was confirmed. Beta-receptor blockade reduced the inotropic effect and almost abolished the chronotropic effect, whereas the vasodilating effect was unaltered. The main haemodynamic effect of secretin was caused by activation of receptors other than the beta-adrenergic receptors.