Objective: Since renal sympathetic nerves are involved in the regulation of sodium excretion, we investigated whether treatment with urapidil, an alpha1-adrenoceptor blocking agent which also lowers sympathetic activity, alters sodium excretory capacity in patients with essential hypertension.
Design: A double-blind, randomized, parallel-group study.
Methods: Studies were carried out in 26 patients who were randomized to treatment with either placebo or urapidil for 8 weeks. Before and after treatment blood pressure, renal haemodynamics and various neurohormones were measured, as well as the response of these variables to a hypertonic saline infusion.
Results: Urapidil had no effect on renal haemodynamics or neurohormones at rest However, as compared to placebo the saline-induced rises in renal plasma flow and glomerular filtration rate lasted longer during treatment with urapidil. Responses of renin, angiotensin II and catecholamines were not modified by urapidil. On the other hand, aldosterone was less suppressed while atrial natriuretic peptide was less stimulated following the saline load when patients had been treated with urapidil. Cumulative sodium excretion during a 3 h period from the moment of saline infusion was similar whether patients had been treated with placebo or with urapidil.
Conclusions: Our data show that urapidil interferes with renal haemodynamics after sodium loading but that any tendency to promote sodium output may be offset by changes in aldosterone and atrial natriuretic peptide. We conclude that urapidil, under the circumstances tested, does not affect the sodium excretory capacity of the kidney.