Neural control of circulation before and after intravenous urapidil in essential hypertension.

Drugs interfering with sympathetic influences on the cardiovascular system have been shown to effectively lower blood pressure in hypertension. However, sympathetic cardiovascular control is involved in blood pressure homeostasis, which means that these drugs may produce potential adverse haemodynamic effects that may reduce the benefit of their antihypertensive action. This paper summarises the results of a study in which we examined the effects of urapidil on the arterial baroreflex and the cardiopulmonary reflex in 6 essential hypertensive patients given 25 mg of the drug intravenously. The dose of the drug used caused a marked reduction in arterial blood pressure (direct measurement). However, pressor and depressor responses to carotid baroreceptor deactivation and stimulation (neck chamber device), respectively, were not modified when compared with those observed in the placebo period. This was also the case for increases and reductions in both forearm vascular resistance and plasma noradrenaline (norepinephrine) concentrations induced by deactivating and stimulating cardiopulmonary receptors, respectively. The pressor and tachycardic responses to handgrip and cold exposure were also unaffected by the drug. It is concluded that when administered at a clinically effective dose urapidil does not adversely affect major reflex mechanisms involved in neural cardiovascular regulation. This has favourable implications for the use of the drug in clinical practice.