Ounis-Skali Nadia, Mitchell Gary F, Solomon Caren G, Solomon Scott D, Seely Ellen W
Endocrinology, Diabetes and Hypertension Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Investig Med. 2006 Sep;54(6):321-6. doi: 10.2310/6650.2006.05055.
Changes in estradiol and progesterone during the human menstrual cycle may impact vascular and cardiac function. Renin-angiotensin-aldosterone system (RAAS) hormones increase during the luteal phase of the menstrual cycle and may antagonize the vascular effects of estradiol. This study was designed to investigate central arterial changes, cardiac function, and RAAS activity in response to gonadal steroid variations during the menstrual cycle.
We studied 15 women during the follicular and midluteal phases with determination of estradiol, progesterone, hormones of the RAAS, and spot urine sodium and creatinine levels. Central pulsatile hemodynamics was evaluated using calibrated carotid tonometry and central aortic Doppler flow. Systolic ejection period (SEP) and systolic pressure time integral (SPTI) were computed from carotid pressure waveforms.
Levels of estradiol, progesterone, and RAAS hormones were higher in the luteal phase. SEP and SPTI were lower during the luteal phase, whereas central and peripheral blood pressures and measures of arterial stiffness were unchanged between the two phases. The urine sodium-to-creatinine ratio was similar at both phases.
Central arterial stiffness does not differ between the follicular and midluteal phases of the menstrual cycle in healthy women, despite significant changes in estradiol and progesterone levels. Systole was shortened during the midluteal phase. RAAS activation during the luteal phase may be responsible for a lack of the expected estradiol-mediated reduction in arterial stiffness between the two phases of the menstrual cycle. Because load was unchanged, the decrease in SEP and SPTI may represent a direct effect of estrogen, progesterone, or RAAS activation on ventricular function.
人类月经周期中雌二醇和孕酮的变化可能会影响血管和心脏功能。肾素-血管紧张素-醛固酮系统（RAAS）激素在月经周期的黄体期会增加，可能会拮抗雌二醇的血管效应。本研究旨在调查月经周期中性腺类固醇变化对中心动脉变化、心脏功能和RAAS活性的影响。
我们对15名女性在卵泡期和黄体中期进行了研究，测定了雌二醇、孕酮、RAAS激素以及随机尿钠和肌酐水平。使用校准的颈动脉张力测量法和中心主动脉多普勒血流评估中心搏动血流动力学。从颈动脉压力波形计算收缩射血期（SEP）和收缩压时间积分（SPTI）。
黄体期雌二醇、孕酮和RAAS激素水平较高。黄体期SEP和SPTI较低，而两个阶段之间的中心和外周血压以及动脉僵硬度测量值没有变化。两个阶段的尿钠肌酐比值相似。
在健康女性中，尽管雌二醇和孕酮水平有显著变化，但月经周期的卵泡期和黄体中期之间中心动脉僵硬度并无差异。黄体中期收缩期缩短。黄体期RAAS激活可能是月经周期两个阶段之间预期的雌二醇介导的动脉僵硬度降低缺乏的原因。由于负荷不变，SEP和SPTI的降低可能代表雌激素、孕酮或RAAS激活对心室功能有直接影响。
