LISINOPRIL REDUCES POSTEXERCISE ALBUMINURIA MORE EFFECTIVELY THAN ATENOLOL IN PRIMARY HYPERTENSION

Physical exercise causes transient albuminuria. The mechanisms of post exercise albuminuria are not fully clarified but stimulation of the re nin-angiotensin system (RAS) probably plays a major role through intra renal haemodynamic changes causing an elevated filtration pressure. In a randomised, double-blind, crossover study we compared the effects o n urinary albumin excretion (UAE) of lisinopril (L) and atenolol (A) t herapy, i.e. we aimed to investigate whether inhibition of the RAS or inhibition of beta(1)-adrenoceptor-mediated effects of the sympathetic nervous system differed with regard to changes in UAE. Sixteen patien ts with uncomplicated primary hypertension were studied. Four standard ised bicycle ergometer exercise tests were performed, before and after each active treatment period. UAE 30 min postexercise, determined by radioimmunoassay, was significantly lowered by both treatments: -278 m u g . min(-1) (L) and -199 mu g . min(-1) (A). The reduction of postex ercise UAE achieved by treatment with the angiotensin-converting enzym e (ACE) inhibitor (L) was significantly greater than that achieved by the beta(1)-selective adrenoceptor blocker treatment. Blood pressure ( BP) at rest and during exercise were equally reduced by both drugs. In conclusion, this study showed that antihypertensive treatment with an ACE inhibitor was more effective in reducing exercise-induced albumin uria than a beta(1)-selective adrenoceptor-blocking agent with a simil ar degree of BP reduction in patients with uncomplicated primary hyper tension. This suggests that the RAS plays a major role in postexercise albuminuria in hypertensive subjects. The clinical significance of th is finding, however, remains to be clarified.