EFFECTS OF MOXONIDINE ON STRESS-INDUCED PEAK BLOOD-PRESSURE AND RENAL-FUNCTION - A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED CROSSOVER STUDY

Moxonidine is an imidazoline I1-receptor agonist that centrally acts b y reducing the sympathetic tone. Furthermore, proximal tubular I1-rece ptors have been isolated in human kidneys, but their natriuretic effec ts have never been demonstrated. Because stress tests elicited a sympa thetically mediated increase in blood pressure and in sodium reabsorpt ion, the aim of this study was to assess the effects of moxonidine (0. 4 mg/day; 1 month) on stress-induced cardiovascular response and renal sodium handling in hypertensives, in a double-blind, crossover, place bo-controlled study. The stress test used is an efficient and reproduc ible computerized version of Stroop's stress test. During the experime ntal sessions, both rest and stress renal functional parameters were d etermined: glomerular filtration rate (inulin clearance), renal plasma flow (para-aminohippurate clearance), filtration fraction, sodium exc retion, and segmental sodium tubular reabsorption (lithium clearance). During the placebo phase, stress induced a significant increase in sy stolic blood pressure (Delta SBP; 15.8 +/- 10.7 mm Hg) and diastolic b lood pressure (Delta DBP; 8.2 +/- 6.1 mm Hg). During stress, glomerula r filtration rate tended to decrease, whereas renal plasma flow signif icantly decreased, resulting in a significant increase in filtration f raction. Despite the increase in BP, stress induced a decrease in sodi um excretion that was mainly due to a non-significant increase in sodi um reabsorption in the proximal parts of the tubules, Moxonidine signi ficantly reduced rest and stress BP, but the stress cardiovascular rea ctivity was not altered. At rest, renal function was well preserved by the treatment. Stress-induced modifications in renal function and sod ium handling were not altered by the treatment. In conclusion, moxonid ine reduced rest and stress-induced peak BP and preserved basal renal function. The study failed to demonstrate any effect of moxonidine eit her on basal renal sodium handling or on stress-induced increase in so dium reabsorption.