RO 363 is an effective inotropic stimulant and is a cardiovascular modulator that decreases diastolic blood pressure and pronounces increases in myocardial contractility. Ro 363 is an effective and highly selective β1-adrenoceptor agonist.

RO 363 is approximately half as effective as (-)-Isoprenaline in tissues where actions are due to β1-receptor activation (guinea-pig atrial and ileal preparations and ventricular strips from the rabbit, rat, and guinea-pig. In spontaneously contracted tracheal preparations from the guinea-pig, RO 363 is a full agonist and is approximately half as potent as (-)-Isoprenaline. These effects of RO 363 are due to the activation of a population of β1-receptors in the tissue since RO 363 and (-)-Isoprenaline have the same relative potencies in trachea, cardiac and ileal preparations. Isolated perfused heart preparations from guinea-pigs developed arrhythmic contractions following the administration of Ro 363 in doses producing 70-100% of its maximal chronotropic responses [1][2].

Ro 363 elicits ventricular arrhythmias following the administration of subarrhythmic doses of ouabain and increases the number of subauricular escape beats which occurred during vagal nerve stimulation in non-ouabain treated animals. In chloralose-anesthetized cats, Ro 363, when compared to epinephrine, is essentially devoid of arrhythmogenic activity in animals in which cardiac sensitization is induced by U-0882 or halothane [1].