Abstract

Objective: Aldosterone induces vascular fibrosis and increases arterial stiffness (AS) of conductance arteries via mineralocorticoid-receptor (MR) activation. In uncomplicated essential hypertensives (EHs) we measured systemic AS at baseline and after chronic administration of MR-antagonist Canrenone. Design and method: Twenty EHs (age 50 ± 12 yrs, M/F = 15/10, clinic BP 159/87 ± 2.4/2.2) on chronic treatment with an ACE inhibitor or angiotensin II antagonist plus hydrochlorothiazide at maximal doses, were randomly assigned to Canrenone 50 or 100 mg/day for 3 months. Blood pressure (BP, sphygmomanometer), heart rate (HR, EKG), stroke volume index (SVI, impedance cardiography) were measured in supine patients before and after Canrenone. AS was assessed as the ratio of pulse pressure (PP) to SVI. Results: Canrenone decreased PP (from 68.7 ± 2.9 to 51.9 ± 2.9 mmHg, means ± sem, p < 0.01) without affecting SVI (33.2 ± 1.4 vs 31.5 ± 1.4 ml/m2) and HR (64.4 ± 1.9 vs 65.5 ± 2.2 bt/min). Thus, AS decreased from 2.14 ± 0.13 to 1.70 ± 0.12 mmHg/ml/m2 (Figure), the decrements induced by low and high canrenone dose being not different (−0.49 ± 0.11 vs −0.39 ± 0.19 mmHg/ml/m2, respectively).Conclusions: Chronic treatment with MR-antagonist Canrenone decreases systemic arterial stiffness in uncomplicated EHs; this effect may improve cardiovascular risk profile in these subjects.

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