Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State Street, Jackson, MS 39216-4505, USA.
Hypertension. 2010 Sep;56(3):359-63. doi: 10.1161/HYPERTENSIONAHA.110.152975. Epub 2010 Aug 2.
After menopause, blood pressure increases in women. However, the underlying mechanisms responsible for postmenopausal hypertension are not completely understood. This study was conducted to determine the role that the renin-angiotensin system (RAS) plays in post-menopausal hypertension. Post-estrous cycling (postmenopausal) spontaneously hypertensive rats or young female controls were treated with losartan, an angiotensin (Ang) II type 1 receptor blocker, for 25 days. Mean arterial pressure was recorded continuously by radiotelemetry. Losartan significantly decreased blood pressure in postmenopausal rats and young female controls but failed to normalize blood pressure in postmenopausal rats to levels found in young controls. Plasma renin activity and plasma angiotensinogen were significantly elevated, and intrarenal Ang II type 1 receptor and renin mRNA expression were significantly downregulated in postmenopausal rats. Therefore, RAS only partially contributes to hypertension in postcycling spontaneously hypertensive rats, whereas hypertension in young females is mediated mainly by the RAS. The data suggest that other mechanisms besides activation of the RAS are likely involved in postmenopausal hypertension.
绝经后,女性的血压会升高。然而,导致绝经后高血压的潜在机制尚不完全清楚。本研究旨在确定肾素-血管紧张素系统(RAS)在绝经后高血压中的作用。用血管紧张素(Ang)II 型 1 受体阻滞剂氯沙坦(losartan)治疗动情周期后(绝经后)自发性高血压大鼠或年轻雌性对照 25 天。通过无线电遥测连续记录平均动脉压。氯沙坦可显著降低绝经后大鼠和年轻雌性对照组的血压,但未能使绝经后大鼠的血压正常化至年轻对照组的水平。绝经后大鼠的血浆肾素活性和血浆血管紧张素原显著升高,肾内 Ang II 型 1 受体和肾素 mRNA 表达显著下调。因此,RAS 仅部分参与了循环后自发性高血压大鼠的高血压,而年轻女性的高血压主要由 RAS 介导。这些数据表明,除了 RAS 的激活外,其他机制可能也与绝经后高血压有关。