caa a22 4500 477057985 CHVBK 20180405111352.0 cr unu---uuuuu 170330e19960101xx s 000 0 eng 10.1007/BF00226326 doi (NATIONALLICENCE)springer-10.1007/BF00226326 Lisinopril reduces postexercise albuminuria more effectively than atenolol in primary hypertension [Elektronische Daten] [C. R»ngemark, T. Hedner, O. Samuelsson, H. Lind, L. Lindholm] Physical exercise causes transient albuminuria. The mechanisms of postexercise albuminuria are not fully clarified but stimulation of the reninangiotensin system (RAS) probably plays a major role through intrarenal haemodynamic changes causing an elevated filtration pressure. In a randomised, double-blind, crossover study we compared the effects on urinary albumin excretion (UAE) of lisinopril (L) and atenolol (A) therapy, i.e. we aimed to investigate whether inhibition of the RAS or inhibition of β1-adrenoceptor-mediated effects of the sympathetic nervous system differed with regard to changes in UAE. Sixteen patients with uncomplicated primary hypertension were studied. Four standardised 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 μg·min-1 (L) and-199 μg·min-1 (A). The reduction of postexercise UAE achieved by treatment with the angiotensin-converting enzyme (ACE) inhibitor (L) was significantly greater than that achieved by the β1-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 albuminuria than a β1-selective adrenoceptor-blocking agent with a similar degree of BP reduction in patients with uncomplicated primary hypertension. This suggests that the RAS plays a major role in postexercise albuminuria in hypertensive subjects. The clinical significance of this finding, however, remains to be clarified. Springer-Verlag, 1996 Lisinopril nationallicence Atenolol nationallicence Hypertension nationallicence urinary albumin excretion nationallicence exercise nationallicence ACE inhibition nationallicence &gb-blockade nationallicence R»ngemark C. Department of Clinical Pharmacology, Sahlgrenska Hospital, University of Göteborg, Göteborg, Sweden aut Hedner T. Department of Clinical Pharmacology, Sahlgrenska Hospital, University of Göteborg, Göteborg, Sweden aut Samuelsson O. Department of Nephrology, Sahlgrenska Hospital, University of Göteborg, S-413 45, Göteborg, Sweden aut Lind H. Health Sciences Centre, University of Lund, Dalby, Sweden aut Lindholm L. Health Sciences Centre, University of Lund, Dalby, Sweden aut European Journal of Clinical Pharmacology Springer-Verlag 49/4(1996-01-01), 267-271 0031-6970 49:4<267 1996 49 228 https://doi.org/10.1007/BF00226326 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00226326 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- R»ngemark C. Department of Clinical Pharmacology, Sahlgrenska Hospital, University of Göteborg, Göteborg, Sweden aut NATIONALLICENCE 700 1- Hedner T. Department of Clinical Pharmacology, Sahlgrenska Hospital, University of Göteborg, Göteborg, Sweden aut NATIONALLICENCE 700 1- Samuelsson O. Department of Nephrology, Sahlgrenska Hospital, University of Göteborg, S-413 45, Göteborg, Sweden aut NATIONALLICENCE 700 1- Lind H. Health Sciences Centre, University of Lund, Dalby, Sweden aut NATIONALLICENCE 700 1- Lindholm L. Health Sciences Centre, University of Lund, Dalby, Sweden aut NATIONALLICENCE 773 0- European Journal of Clinical Pharmacology Springer-Verlag 49/4(1996-01-01), 267-271 0031-6970 49:4<267 1996 49 228 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer