The hemodynamic and electrophysiologic effects of rilmenidine were examined after single oral administration to hypertensive patients. In 8 untreated hypertensive patients, cardiac output, pulmonary pressure and blood pressure were measured before and for 10 hours after the administration of 25 micrograms/kg of rilmenidine (1.3 to 2.4 mg, mean 1.88). In addition, electrophysiologic investigations were performed before and 2 hours after administration. Hemodynamics were repeated in 8 other hypertensive patients receiving 50 micrograms/kg rilmenidine (3.0 to 4.8 mg, mean 3.85 mg). The electrophysiologic study was repeated in 8 other hypertensive patients receiving 50 micrograms/kg of rilmenidine (3.2 to 4.4 mg, mean 3.90). In contrast to the results obtained at the dose of 50 micrograms/kg, there was no significant variation in pulmonary arterial pressure, cardiac index or stroke index after administration of 25 micrograms/kg. No significant variation was observed in heart rate, sinus function, conduction parameters or atrial, nodal and ventricular refractory periods after administration of 25 and 50 micrograms/kg. Rilmenidine, after single oral administration at the 25 micrograms/kg dose, led to a significant reduction in blood pressure and peripheral resistance without any significant change in cardiac output; the 25- and 50-micrograms/kg doses led to no alteration in heart rate and cardiac electrophysiology.