Background: In animal experiments, aldosterone has been shown to substantially contribute to the accumulation of collagen fibres in the arterial wall, which can increase arterial stiffness. The aim of the study was to examine the above relationships in human hypertension.

Methods: The study group included 50 hypertensive patients (mean age = 56.8 years, 16/34 M/F) and 29 normotensive controls (mean age = 54.6 years, 15/14 M/F). A Sphygmocor device was used to measure the carotid, radial and aortic augmentation index (AIx) of systolic blood pressure, as well as the aortic pulse wave velocity (PWV). 24-hour urinary aldosterone excretion was assessed. The plasma levels of collagen synthesis marker - procollagen type III amino-terminal peptide (PIIINP) were evaluated.

Results: Hypertensive patients as compared to normotensive controls had higher carotid AIx (142.8 ± 25.2 vs 124.2 ± 24.7%; p = 0.004), higher aortic AIx (39.4 ± 10.1 vs 30.8 ± 13.5%; p=0.005), and higher PWV (9.57 ± 2.86 vs 8.58 ± 1.51 m/sec; p=0.05). With adjustments applied for age, gender, body height, mean arterial pressure and current smoking, 24-hour urinary aldosterone excretion correlated positively with carotid AIx (r=+0.22; p=0.05) and aortic AIx (r=+0.19; p=0.09). We observed also positive correlations between plasma level of PIIINP and carotid AIx (r=+0.20; p=0.06) and aortic Aix (r=+0.24; p=0.05).

Conclusion: In our study group, aldosterone excretion tended to correlate to carotid and aortic, but not radial, augmentation index. The increased arterial stiffness in hypertensive patients could be caused by the deleterious effects of aldosterone excess on the fibrosis and remodeling of the arterial wall, as assessed by circulating PIIINP.