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In spontaneously hypertensive rats resistance artery structure, endothelial dysfunction and geometry-independent wall stiffness were reduced by an angiotensin AT(1)-receptor antagonist. In previous studies of human hypertension, interruption of the renin-angiotensin system corrected small artery structure and endothelial dysfunction, whereas the beta-blocker atenolol did not. We hypothesized that the AT(1)R antagonist losartan, but not the beta-blocker atenolol, would reduce stiffness of gluteal subcutaneous small arteries in essential hypertensive patients. Seventeen untreated mild essential hypertensive patients (47+/-2 years; 75% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for one year. Small, resistance size arteries were studied on pressurized myographs. Blood pressure (mmHg) was reduced (p&lt;0.01) from 145 +/- 4/101 +/- 2 and 147 +/- 6/98 +/- 2 to 128 +/- 4/86 +/- 2 and 131 +/- 3/84 +/- 1 by losartan and atenolol, respectively. The media/lumen ratio of small arteries was unaffected by atenolol (8.3+/-0.3% before and 8.8+/-0.5% after treatment). In contrast, losartan reduced media/lumen ratio from 8.4+/-0.4% to 6.7+/-0.3% (p&lt;0.01). Whereas isobaric elastic modulus was unaffected by either treatment, geometry-independent stiffness (slope of elastic modulus vs. stress) was reduced from 9.7+/-1.2 to 6.1+/-0.9 (P&lt;0.05) under losartan treatment, but was unchanged by atenolol (8.2+/-1.3 to 7.8+/-0.6). In conclusion, treatment with losartan reduced stiffness and structural alterations of subcutaneous resistance arteries of previously untreated essential hypertensive patients, whereas atenolol failed to do so.

Reduction of resistance artery stiffness by treatment with the AT1-receptor antagonist losartan in essential hypertension