The positive inotropic effects of epinine and dopamine have been studied in isolated preparations obtained from human heart in the absence and in the presence of the selective beta adrenoceptors antagonists practolol and ICI 118,551. ED50 values of the two agonists were similar (about 3 x 10(-5) M). The inotropic efficacy of epinine was significantly higher than that of dopamine in adult ventricular and papillary muscles, it was similar to that of dopamine in juvenile myocardial preparations and in adult atria and pectinate muscles. The dopamine-evoked response was significantly more sensitive to practolol than epinine-evoked response, but it was less sensitive to ICI 118,551. pA2 values of practolol and ICI 118,551 were considerably different with epinine but not with dopamine as agonist. The results indicate that, compared to dopamine in isolated human heart preparations, epinine was more potent at beta-2 relative to beta-1 adrenoceptors.

Amlodipine, a dihydropyridine calcium antagonist has been examined on the rhythmic activity of isolated human coronary arteries. Amlodipine inhibited both the spontaneous rhythmic activity and the rhythmic activity evoked by prostaglandin F2 alpha and endothelin in isolated human coronary arteries. It also inhibited the contraction evoked by potassium depolarization. The action of amlodipine was characterized by slow onset and voltage dependency.

We have studied the action of nifedipine and nisoldipine on the contractile activity of human isolated coronary arteries and human isolated auricular and ventricular muscles. Nisoldipine depressed dose dependently the spontaneous rhythmic contractions displayed by the coronary artery preparations and at 1 nM abolished these contractions. Nisoldipine was twenty times more potent than nifedipine as an inhibitor of increase in tone induced by depolarization (100 mM K+). The rhythmic activity induced by serotonin (10 microM) was about five times more sensitive to nisoldipine than to nifedipine. In both auricular and ventricular preparations, isoprenaline evoked an increase in the rate of force development and in the rate of relaxation. Nifedipine was five times (ventricular muscles) and ten times (auricular muscles) more potent than nisoldipine as a negative inotropic agent. The present observations in human isolated preparations indicate that nisoldipine shows a higher vascular selectivity than nifedipine.