Effects of rilmenidine on stress-induced peak blood pressure and renal function

Rilmenidine is an imidazoline I1-receptor agonist that centrally acts by re ducing the sympathetic tone. There is strong experimental evidence that nat riuresis could be evoked by proximal tubular I1-receptors that have also be en isolated in human kidneys. However, in humans, the natriuretic effects o f proximal tubular I1-receptors have never been demonstrated. Because stres s tests elicited a sympathetically mediated increase in blood pressure and in sodium reabsorption, this study examined whether a short-term infusion o f rilmenidine (1 mg) may interfere with stress-induced cardiovascular respo nse and renal sodium handling in normotensive men, in a double-blind, cross over, placebo-controlled study. The stress test used is an efficient and re producible computerized version of the Stroop's stress test. During the exp erimental sessions, both basal and stress renal functional parameters were determined: glomerular filtration rate, renal plasma flow, filtration fract ion, sodium excretion, and segmental sodium tubular reabsorption (lithium c learance). During the placebo phase, stress induced a significant increase in systolic blood pressure (SBP; 22.2 +/- 10.1 mm Hg) and diastolic blood p ressure (DBP; 11.0 +/- 5.0 mm Hg). During stress, glomerular filtration rat e and renal plasma flow tended to decrease, resulting in a nonsignificant i ncrease in filtration fraction. Despite the increase in BP, stress induced a significant decrease in sodium excretion that was due mainly to a nonsign ificant increase in sodium reabsorption in the proximal parts of the tubule s. Rilmenidine significantly reduced rest and stress BP, but the cardiovasc ular reactivity to stress was not altered. The treatment slightly decreased basal glomerular filtration rate and increased renal plasma flow, so that the filtration fraction significantly decreased. The treatment-related de c rease in BP was associated with a significant increase in basal sodium reab sorption. Stress-induced modifications in renal function and sodium handlin g were not altered by the treatment. In conclusion; rilmenidine reduced res t BP and preserved stress-induced reactivity in BP and heart rate. Renal ef fects of rilmenidine are characterized by a decrease in glomerular filtrati on rate and in filtration fraction and an increase in sodium reabsorption. The study failed to demonstrate any effect of rilmenidine on stress-induced increase in sodium reabsorption.