Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE 19716, USA.
J Physiol. 2013 May 1;591(9):2345-55. doi: 10.1113/jphysiol.2012.247882. Epub 2013 Feb 11.
The impact of 17β-oestradiol (E2) exposure on autonomic control of orthostasis in young women is unclear. We tested the hypothesis that autonomic cardiovascular regulation is more sensitive to E2 exposure in women with low orthostatic tolerance. Women underwent an initial maximal lower body negative pressure (LBNP) test to place them into a low (LT, n = 7, 22 ± 1 years old, body mass index 22 ± 1 kg m(-2)) or a high orthostatic tolerance group (HT, n = 7, 22 ± 1 years old, body mass index 24 ± 1 kg m(-2)). We then suppressed endogenous reproductive hormone production using a gonadotrophin-releasing hormone antagonist (GnRHant) for 10 days, with E2 administration during the last 7 days of GnRHant. We measured R-R interval and beat-by-beat blood pressure during the modified Oxford protocol, and changes in heart rate, blood pressure and forearm vascular resistance (FVR) during submaximal LBNP. During submaximal LBNP, FVR increased in HT (ANOVA P < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all levels of LBNP (P < 0.05). Compared with GnRHant, E2 administration shifted FVR lower in LT (ANOVA P < 0.05), with no effect in HT. Administration of E2 increased baroreflex control of heart rate (derived from the modified Oxford protocol) in LT (GnRHant 10.7 ± 2.5 ms mmHg(-1) vs. E2 16.1 ± 2.4 ms mmHg(-1), P < 0.05) but not in HT (GnRHant 13.4 ± 1.9 ms mmHg(-1) vs. E2 15.3 ± 2.4 ms mmHg(-1), n.s.). In conclusion, blunted peripheral vasoconstriction and lower stroke volume contribute to compromised orthostatic tolerance in women; this inability to vasoconstrict is further exacerbated by exposure to E2. Furthermore, E2 administration increases baroreflex-mediated heart rate responses to orthostasis in low orthostatic tolerant women, which is likely to be a compensatory mechanism for the blunted peripheral vascular resistance and lower central volume.
17β-雌二醇（E2）暴露对年轻女性体位性自主神经控制的影响尚不清楚。我们假设，自主心血管调节对低体位耐受性女性的 E2 暴露更为敏感。女性接受了初始最大下体负压（LBNP）测试，将其分为低（LT，n = 7，22 ± 1 岁，体重指数 22 ± 1 kg m(-2))或高体位耐受性组（HT，n = 7，22 ± 1 岁，体重指数 24 ± 1 kg m(-2))。然后，我们使用促性腺激素释放激素拮抗剂（GnRHant）抑制内源性生殖激素产生 10 天，并在 GnRHant 的最后 7 天内给予 E2。我们在改良牛津方案中测量了 R-R 间期和逐搏血压，并在亚最大 LBNP 期间测量了心率、血压和前臂血管阻力（FVR）的变化。在亚最大 LBNP 期间，HT 中的 FVR 增加（ANOVA P < 0.05），而 LT 中 FVR 没有增加（ANOVA P > 0.05），并且在所有 LBNP 水平下，LT 的每搏量均低于 HT（P < 0.05）。与 GnRHant 相比，E2 给药使 LT 的 FVR 降低（ANOVA P < 0.05），而 HT 则没有影响。E2 给药增加了 LT 中的压力反射心率控制（来自改良的牛津方案）（GnRHant 10.7 ± 2.5 ms mmHg(-1) vs. E2 16.1 ± 2.4 ms mmHg(-1)，P < 0.05），但 HT 中没有影响（GnRHant 13.4 ± 1.9 ms mmHg(-1) vs. E2 15.3 ± 2.4 ms mmHg(-1)，n.s.）。总之，外周血管收缩减弱和每搏量降低导致女性体位耐受性受损；这种不能收缩的能力因暴露于 E2 而进一步加剧。此外，E2 给药增加了低体位耐受女性对体位的压力反射介导的心率反应，这可能是外周血管阻力降低和中心容积降低的代偿机制。
