Abstract

Objective: To estimate the effect of moxonidine versus bisoprolol on cellular senescence processes in postmenopausal women with arterial hypertension (AH). Design and method: There was an open randomized control study. The study group was represented by 56 women with AH and a mean age of 63 ± 9.217 years, with SBP of 146.72 ± 7.127 mm Hg and DBP of 84.38 ± 7.941 mm Hg, who received moxonidine treatment (average dose 0.515 mg/day [0.4; 0.6]) for 12 months. The control group was comprised of 59 female patients with AH and a mean age of 61 ± 9.117 years, with SBP of 145.59 ± 6.102 mm Hg and DBP of 86.18 ± 6.682 mm Hg, who received treatment with bisoprolol (average dose 5.0 mg/day [5.0; 7.5]) for 12 months. For all patients, the measurement of telomerase activity was performed using genomic DNA real-time PCR at baseline and after 12 months of treatment. Statistical analysis was carried out using the SPSS/PASW Statistics software (version 18, SPSS Inc., Chicago, Illinois, USA). Results: In both groups there was a substantial and significant BP reduction, in the moxonidine treatment group: SBP – 126.93 ± 8.086 mm Hg (p < 0.001), DBP – 73.64 ± 7.522 mm Hg (p < 0.001); in the bisoprolol treatment group: SBP – 125.83 ± 8.097 mm Hg (p < 0.001), DBP – 73.31 ± 7.964 mm Hg (p < 0.001). Patients from the moxonidine treatment group demonstrated a significant reduction of body weight, on average, by 1.89% (from 75.7 ± 12.77 kg to 74.5 ± 11.7 kg,p < 0.001) and of BMI (from 29.359 ± 4.7 kg/m2 to 28.6 ± 4.4 kg/m2, p < 0.001). By contrast, in the bisoprolol treatment group patients’ average body weight increased by 2.22% (from 76.655 ± 13.754 kg to 78.13 ± 13.728 kg, p < 0.001) as well as BMI (from 29.037 ± 4.6 kg/m2 to 29.609 ± 4.7 kg/m2, p < 0.001). TA in the moxonidine treatment group increased from 0.87 [0.16; 1.18] to 1.1 [0.74; 1.5] (p < 0.001), and, conversely in the bisoprolol treatment group TA decreased from 1.1 [0.5; 1.6] to 0.94 [0.56; 1.5] (p < 0.001). Conclusions: The preliminary data suggests that moxonidine can be used as telomerase activator and effective geroprotective agent. Increased TA against the backdrop of moxonidine treatment may be explained by increased insulin sensitivity, decreased body weight, and, consequently, lower intensity of chronic inflammation.

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