A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Treatment of postmenopausal hypertension with moxonidine, a selective imidazoline receptor agonist
Tekijät: Kaaja R, Manhem K, Tuomilehto J
Julkaisuvuosi: 2004
Journal: International Journal of Clinical Practice -Supplement-
Tietokannassa oleva lehden nimi: International journal of clinical practice. Supplement
Lehden akronyymi: Int J Clin Pract Suppl
Numero: 139
Aloitussivu: 26
Lopetussivu: 32
Sivujen määrä: 7
ISSN: 1368-504X
Tiivistelmä
This study compared the effects of two sympatholytic agents--one central (moxonidine) and one peripheral (atenolol)--on blood pressure and other metabolic syndrome factors in postmenopausal hypertensive women who were not taking hormone replacement therapy. Atenolol and moxonidine led to a statistically significant reduction in diastolic blood pressure of 9.5 mmHg and 5.5 mmHg, respectively. A clear rebound effect was observed in the atenolol patients whereas the moxonidine group exhibited a slightly further decrease in blood pressure. Moxonidine also caused a profound decrease in both mean plasma-glucose area under the curve (AUC) during oral glucose tolerance test (-0.96 mmol/L x H, NS) and mean plasma-insulin AUC (-6.15 mU/L x H). Therefore, moxonidine displayed a slightly less potent antihypertensive effect than atenolol in hypertensive postmenopausal women, but it demonstrated a better metabolic effect. To conclude, moxonidine could benefit hypertensive postmenopausal women who display other signs of metabolic syndrome.
This study compared the effects of two sympatholytic agents--one central (moxonidine) and one peripheral (atenolol)--on blood pressure and other metabolic syndrome factors in postmenopausal hypertensive women who were not taking hormone replacement therapy. Atenolol and moxonidine led to a statistically significant reduction in diastolic blood pressure of 9.5 mmHg and 5.5 mmHg, respectively. A clear rebound effect was observed in the atenolol patients whereas the moxonidine group exhibited a slightly further decrease in blood pressure. Moxonidine also caused a profound decrease in both mean plasma-glucose area under the curve (AUC) during oral glucose tolerance test (-0.96 mmol/L x H, NS) and mean plasma-insulin AUC (-6.15 mU/L x H). Therefore, moxonidine displayed a slightly less potent antihypertensive effect than atenolol in hypertensive postmenopausal women, but it demonstrated a better metabolic effect. To conclude, moxonidine could benefit hypertensive postmenopausal women who display other signs of metabolic syndrome.
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