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This study evaluates the effect of moxonidine versus bisoprolol on collagen type 1 C-telopeptide in postmenopausal female patients with arterial hypertension and osteopenia.
Full description
Several experimental studies have demonstrated that moxonidine may lower the activity of Na+- independent Cl-/bicarbonate exchanger (anion exchanger, AE) which plays an essential role in viability of osteoclasts that are crucial for bone resorption. The suppression of AE proteins activity has been proven to inhibit osteoclast activity and reduce bone resorption whereas the moxonidine molecule is known to reduce the AE protein activity. Therefore, the results of experimental studies have shown the ability of moxonidine to inhibit bone resorption through its effect on the osteoclast activity.
Published data contain information on positive effects of beta-blockers on the bone tissue condition. There are data which clearly demonstrate a positive effect of beta-blockers on bone mass.
The proposed trial is a comprehensive study of moxonidine effects on processes of cellular and vascular aging as well as bone metabolism.
Enrollment
Sex
Volunteers
Inclusion criteria
Female with age 45 years and older.
Postmenopausal (absence of menstrual periods for a minimum of 12 months) at the moment of Informed Consent sign.
Arterial hypertension grade I / II per ESH/ESC 2013 guidelines (diastolic pressure ≥ 90 and <110 mm Hg, systolic pressure ≥140 and <180 mm Hg).
Not achieving BP targets <140/90 mmHg either during antihypertensive therapy or naive.
Absence of moxonidine or bisoprolol treatment at least 6 months before the study
Osteopenia of lumbar spine and/or proximal part of the femur (osteoporosis T-score from -1 to -2.5 standard deviations [SD]) by X-Ray densitometry.
Signed Informed Consent for participation in the study
Exclusion criteria
Hypersensitivity to moxonidine, bisoprolol or any other ingredient of the respective formulations
Any Contraindications for moxonidine, bisoprolol
Osteoporosis (Т-score below - 2.5 SD).
Primary or secondary hyperparathyroidism.
Paget's disease of bones.
History of low traumatic bone fractures.
Malabsorption syndrome.
History of gastro-intestinal surgery.
Severe disturbance of peripheral circulation.
Raynaud's disease.
Symptomatic (secondary) hypertension (caused by any primary internal diseases)
Morbid obesity (BMI over 40 kg/m2).
Symptoms of estrogen deficiency such as hot flushes, nights sweat, vaginal dryness
Administration of any hormone-replacement therapy (HRT) or intake of isoflavones
Secondary hypogonadism.
Sistolic BP ≥180 mm Hg and/or Diastolic BP ≥110 mm Hg.
Clinical presentations of cardiovascular disease: coronary heart disease (CHD), history of stroke, transient ischemic attack (TIA), Charcot's syndrome.
Severe heart failure.
Hemodynamically significant congenital heart disease.
Heart rhythm disorders which require permanent use of any antiarrhythmic medications (including β-adrenoblockers and calcium antagonists).
Diabetes mellitus of any genesis.
Severe liver failure.
Severe kidney failure including patients on dialysis
Thyroid diseases accompanied by functional disorders (thyrotoxicosis or uncompensated hypothyroidism).
Alcohol and drug abuse.
Patients with oncological diseases diagnosed within 5 years before IC execution.
Inability of the patient to comprehend the essence of the program and to provide his/her consent for participation in the program.
Patients with any condition, which in the opinion of the Investigator makes the patient unsuitable for inclusion based on clinical judgment.
Corticosteroid therapy
Participation in any other clinical study during the whole course of this investigation including participation in a study within 30 days prior to providing the informed consent for this trial
Primary purpose
Allocation
Interventional model
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114 participants in 2 patient groups
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Data sourced from clinicaltrials.gov
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