Central sympatholytic therapy has anti-inflammatory properties in hypertensive postmenopausal women

• DOI: 10.1097/hjh.0b013e328311cf37
• Publication Date: 2008-11-07T08:09:59Z
• Authors: Maritta K Pöyhöne...; Karin Manhem; Per Katzman; Aleksandras Kibar...; Riitta L Antikainen; Risto U Erkkola; Jaakko O Tuomilehto; Pertti E Ebeling; Risto J Kaaja
• Keywords: Inflammation; Sweden; Interleukin-6; Imidazoles; Lithuania; Middle Aged; Overweight; 3. Good health; Postmenopause; 03 medical and health sciences; C-Reactive Protein; 0302 clinical medicine; Atenolol; Double-Blind Method; Hypertension; Humans; Receptors, Tumor Necrosis Factor, Type II; Female; Adiponectin; Prospective Studies; Insulin Resistance; Antihypertensive Agents; Finland

Postmenopausal phase expresses many unfavourable physiological changes that lead to increased risk for cardiovascular disease. We compared the effect of two sympatholytic antihypertensive drug treatments, the centrally acting imidazoline receptor-1 agonist moxonidine and peripherally acting beta-blocking agent atenolol on sensitive inflammatory markers in overweight postmenopausal women with diastolic hypertension.This was a multicentre, multinational double-blinded, prospective study comparing moxonidine (0.3 mg twice daily) with atenolol (50 mg once daily) in 87 hypertensive postmenopausal overweight women who were not taking hormone therapy. Sensitive C-reactive protein, IL-6, TNFalpha, TNFalpha-RII and adiponectin were determined in the beginning of the study and after 8 weeks of medical treatment.TNFalpha increased in atenolol and decreased in moxonidine group (P = 0.0004 between the groups). Adiponectin concentration decreased dramatically in atenonol but did not change in moxonidine treatment group (P < 0.0001 between the groups). In logistic regression analysis only treatment group showed an independent effect on changes in adiponectin and TNFalpha concentrations.We believe that centrally acting sympatholytic agent moxonidine is beneficial in the treatment of postmenopausal women with hypertension by reducing inflammatory cytokine TNFalpha without changing protective adiponectin level.