Hemodynamic and neural effects of urapidil and prazosin in essential hypertensives.

Assessment of the effects of antihypertensive drugs on sympathetic cardiovascular modulation is aimed not only at exploring the neural mechanisms of the hypotensive action of different pharmacological compounds but also at evaluating the effects of these drugs on neural cardiovascular homeostatic control. This paper, after reviewing the effects of different antihypertensive drugs on efferent postganglionic muscle sympathetic nerve activity directly assessed in man via the microneurographic technique, will report the preliminary results of a study we have recently performed in 12 untreated mild essential hypertensives. This study was aimed at examining the effects of a single oral administration of either the hybrid drug urapidil (30 mg) or the pure alpha-blocker prazosin (2 mg) on arterial blood pressure (Finapres technique), heart rate (electrocardiogram) and muscle sympathetic nerve activity (microneurography at the peroneal nerve). For similar blood pressure reductions, urapidil caused a lesser degree of tachycardia in comparison with prazosin (+5.1 +/- 1.2 vs +8.4 +/- 0.8 beats/min, p < 0.05) but superimposable increases in muscle sympathetic nerve traffic (+15.4 +/- 2.8 vs 17.5 +/- 3.5 bursts/min). These results suggest that the two drugs induce similar degrees of blood pressure reduction as well as of muscle sympathetic activation. Urapidil, however, is accompanied by less tachycardia than prazosin, presumably because of a selective drug's action on either parasympathetic or sympathetic modulation of heart rate, triggered by the stimulation of central 5HT1A-receptors.