Prazosin is a prototype selective a antagonist dilates both resistance and capacitance vessels; effect on the former predominating. The haemodynamic effects—reduction in t.p.r. and mean BP with only slight decrease in venous return and c.o. are similar to that produced by a direct acting vasodilator. However, there is little reflex cardiac stimulation and renin release during long-term therapy of prazosin. Tachycardia does not compensate for the fall in BP, because release inhibitory a2 (presynaptic) receptors are not blocked: autoregulation of NA release remains intact. Prazosin probably decreases central sympathetic tone also.

Renal blood flow and g.f.r. are maintained but fluid retention may attend hypotension. Cardiovascular reflexes are not appreciably impaired by chronic therapy, but postural hypotension and fainting may occur in the beginning—called ‘first dose effect’, and with dose increments. This disappears with continued therapy, but may persist in the elderly. For this reason, prazosin is always started at low dose (0.5 mg) given at bedtime and gradually increased with twice daily administration till an adequate response is produced (max. dose 10 mg BD). Patients who develop marked first dose effect with prazosin generally require lower maintenance doses (2—6 mg/ day).

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