Presse médicale (Paris, France : 1983) vol:19 issue:30 pages:1407-11
In hypertensive patients as well as in normal subjects, urapidil has a hypotensive action. This is mainly mediated by a peripheral alpha adrenoceptor blockade with a decrease in systemic vascular resistance. In addition, acute animal experiments demonstrated a centrally mediated hypotensive action, possibly by 5-hydroxytryptamine1A-receptor stimulation. Studies in humans showed an increase in cardiac output, which was not always significant; it resulted either from an increased heart rate or an increased stroke volume. Acute changes in pulmonary hemodynamics after administration of urapidil were most pronounced in patients with pulmonary hypertension: pulmonary artery pressure and pulmonary vascular resistance decreased significantly and pulmonary capillary wedge pressure decreased non-significantly. A small reduction in pulmonary artery pressure and capillary wedge pressure was seen in patients with congestive heart failure and in patients in whom acute blood pressure elevation developed after coronary bypass surgery. In patients with essential hypertension, forearm, renal and splanchnic flows were shown to increase and vascular resistance to decrease significantly after an acute intravenous doses of urapidil. The hemodynamic changes that occur during chronic therapy are largely unknown, except for systemic vascular resistance which remains decreased.