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CLINICAL STUDIES |
From the Institute of Clinical Pharmacology, Medical Faculty, University of Technology, Dresden, Germany (Dr Schindler, Dr Bramlage, Dr Maywald, Dr Oertel, Dr Kirch); Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina (Dr Brosnihan, Dr Ferrario); and the Institute of Medical Computer Science and Biometrics, Medical Faculty, University of Technology, Dresden, Germany (Dr Koch).
Experimental studies point to an interplay between hypercholesterolemia and hypertension, acting through the renin angiotensin system. In a crossover study design with 8 healthy subjects, the authors tested the hypothesis that statin treatment exerts renin angiotensin system-modulating effects in veins by down-regulation of AT1-receptors, resulting in reduced Angiotensin II (Ang II)-induced venoconstriction and by increasing the pleiotropic Ang II-metabolite Ang-(1-7). Irbesartan was used as positive control. Ang II-induced venoconstriction was 49% ± 9% before and 64% ± 10% after 30 days of atorvastatin treatment compared to 50% ± 8% before and 15% ± 9% after irbesartan (P = .004). Plasma angiotensin levels significantly increased only after irbesartan treatment (Ang II: 35 ± 4 vs 329 ± 101 pg/mL [P = .02]; Ang-(1-7): 10 ± 3 vs 35 ± 6 pg/mL [P = .01]) compared to atorvastatin treatment (Ang II: 26 ± 5 vs 31 ± 4 pg/mL [P = ns]; Ang-(1-7): 9 ± 2 vs 11 ± 3 pg/mL [P = ns]). The data indicate that atorvastatin does not inhibit Ang II-induced venoconstriction in vivo and point toward a supportive role of Ang-(1-7) in contributing to the antihypertensive and beneficial vascular effects of irbesartan.
Key Words: AT1 receptor • statin • renin angiotensin aldosteron system • veins • Angiotensin-(1-7)
Address for reprints: Christoph Schindler, MD, Institute of Clinical Pharmacology, Medical Faculty of the University of Technology, Fiedlerstrasse 27, D-01307 Dresden, Germany; e-mail: christoph.schindler{at}tu-dresden.de.
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