Response to Testosterone and sympathetic nerve activity during pregnancy.

Response to Testosterone and sympathetic nerve activity during pregnancy.
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怀孕期间对睾酮和交感神经活动的反应。

DOI:
10.1161/hypertensionaha.113.01216
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发表时间:
2013
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Sathishkumar,Kunju
Sathishkumar,Kunju
中科院分区:
--
文献类型:
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作者:
Chinnathambi,Vijayakumar;Balakrishnan,Meena;Ramadoss,Jayanth;Yallampalli,Chandrasekhar;Sathishkumar,Kunju

文献摘要

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我怀着极大的兴趣阅读了Chinnathambi等人的文章,该文章研究了睾酮对内皮一氧化氮(NO)系统的影响。睾酮在妊娠期心血管功能中的作用尚未得到充分研究,尽管事实上,在先兆子痫和多囊卵巢综合征妊娠中睾酮水平被夸大。Chinnathambi等人1使用了一种对照良好的实验模型,其中妊娠大鼠注射了溶剂或丙酸睾酮,目的是增加血浆睾酮,以模拟先兆子痫期间观察到的水平。作者报告说,睾酮增加与血压升高和NO介导的血管舒张作用减弱有关。这项新的研究为妊娠期高血压提供了重要的机制见解和潜在的治疗靶点。一些研究表明,妊娠与肌肉交感神经活动水平增加有关,越来越多的证据表明,先兆子痫可能与这种交感神经兴奋伴随着血管舒张机制功能障碍的情况有关。2此外,Sverrisdottir等3报道多囊卵巢综合征与静息肌交感神经活动升高相关,交感神经兴奋程度与睾酮水平显著相关。因此,这似乎是合理的,除了削弱NO介导的血管舒张,睾酮也可能增加与怀孕相关的肌肉交感神经活动的典型激增。到目前为止,睾酮对妊娠期肌肉交感神经活动的影响尚未得到充分研究,目前仍不清楚异常高水平的睾酮是否会加重与妊娠相关的交感神经风暴。此外,阻塞性睡眠呼吸暂停(OSA)是公认的高血压危险因素。有证据表明,怀孕增加了OSA的发病率,先兆子痫可能会加重OSA的严重程度。4如Chinnathambi等人所强调的,1在先兆子痫期间,睾酮升高了约2倍。最近的研究表明,多囊卵巢综合征女性中OSA的患病率也是男性的5 - 10倍。
I read with great interest the article by Chinnathambi et al1 that examined the influence of testosterone on the endothelial nitric oxide (NO) system. The role of testosterone in gestational cardiovascular function has not been adequately examined, despite the fact that testosterone levels are exaggerated in preeclamptic and polycystic ovary syndrome pregnancies. Chinnathambi et al1 used a well-controlled experimental model in which pregnant rats were injected with vehicle or testosterone propionate, with the goal of increasing plasma testosterone to mimic levels observed during preeclampsia. The authors report that increased testosterone was associated with elevated blood pressure and blunted NO-mediated vasodilation. This novel study provides critical mechanistic insight and a potential therapeutic target during gestational hypertension.Several studies suggest that pregnancy is associated with increased levels of muscle sympathetic nerve activity, and evidence is accumulating to suggest that preeclampsia might be linked to circumstances, where this sympathoexcitation is accompanied by dysfunction of vasodilatory mechanisms. 2 Moreover, Sverrisdottir et al3 reported that polycystic ovary syndrome was associated with elevated resting muscle sympathetic nerve activity, and that the extent of sympathoexcitation was significantly related to testosterone levels. Therefore, it seems plausible that in addition to impairing NO-mediated vasodilation, 1 testosterone might also augment the typical surge of muscle sympathetic nerve activity associated with pregnancy. To date, the influence of testosterone on gestational muscle sympathetic nerve activity has not been adequately examined, and it remains unclear whether abnormally high levels of testosterone worsen the sympathetic storm associated with pregnancy. In addition, obstructive sleep apnea (OSA) is a recognized risk factor for hypertension. Evidence suggests that pregnancy increases the incidence of OSA, and that preeclampsia may exacerbate OSA severity. 4 As highlighted by Chinnathambi et al, 1 testosterone is elevated≈ 2-fold during preeclampsia. Recent studies suggest that OSA is also≥ 5 to 10 times more prevalent in polycystic ovary syndrome women compared with