The forearm vascular response to sympathetic activation is attenuated in female, but not male, participants following acute intermittent hypoxia.

The forearm vascular response to sympathetic activation is attenuated in female, but not male, participants following acute intermittent hypoxia.
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急性间歇性缺氧后,女性参与者的前臂血管对交感神经激活的反应减弱,但男性参与者则不然。

DOI:
10.1152/japplphysiol.00760.2022
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发表时间:
2023
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Limberg,JacquelineK
Limberg,JacquelineK
中科院分区:
--
文献类型:
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作者:
Jacob,DainW;Morgenthaler,LeandraD;Harper,JenniferL;Limberg,JacquelineK

文献摘要

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急性暴露于缺氧促进交感神经系统活动(SNA)和局部血管舒张的增加。在啮齿类动物中,间歇性缺氧(IH)介导的SNA增加与男性而非女性的血压升高相关;值得注意的是,卵巢切除术后女性性别的保护作用丧失。这些数据表明,血管反应缺氧和/或SNA以下IH可能是性别和/或激素特异性,但机制尚不清楚。我们假设缺氧介导的血管舒张和SNA介导的血管收缩在成年男性急性IH后不会改变。我们进一步假设,急性IH后,女性成年人的缺氧性血管舒张功能会增强,SNA介导的血管收缩功能会减弱,内源性雌二醇高时效果最大。12名男性(25 ± 1岁)和10名女性(25 ± 1岁)参与者接受了30分钟的IH。在低(卵泡早期)和高(卵泡晚期)雌二醇状态下研究雌性动物。在IH之前和之后,参与者完成了两项试验[稳态缺氧和冷加压试验(CPT)],其中测量前臂血流量和血压并用于确定前臂血管传导性(FVC)。雄性IH后FVC对缺氧的反应(P= 0.67)和交感神经激活(P= 0.73)无变化。无论雌二醇状态如何,IH对女性缺氧性血管舒张没有影响(P= 0.75)。与此相反,血管反应交感神经激活减弱后IH(P= 0.02),独立于雌二醇状态(P= 0.65)的女性。目前的数据突出性别相关的差异,神经血管反应性急性IH。新&值得注意的是,我们研究了急性间歇性缺氧(AIH)对交感神经激活和急性缺氧的血管反应的影响。目前的研究结果表明,尽管AIH对缺氧的血管反应没有影响,但在AIH后的女性中,前臂对急性交感神经激活的血管收缩反应减弱,与雌二醇状态无关。这些数据提供了对AIH潜在益处的机械理解,以及生物性别的影响。
Acute exposure to hypoxia promotes both an increase in sympathetic nervous system activity (SNA) and local vasodilation. In rodents, intermittent hypoxia (IH)-mediated increases in SNA are associated with an increase in blood pressure in males but not females; notably, the protective effect of female sex is lost following ovariectomy. These data suggest the vascular response to hypoxia and/or SNA following IH may be sex- and/or hormone specific—although mechanisms are unclear. We hypothesized that hypoxia-mediated vasodilation and SNA-mediated vasoconstriction would be unchanged following acute IH in male adults. We further hypothesized that hypoxic vasodilation would be augmented and SNA-mediated vasoconstriction would be attenuated in female adults following acute IH, with the greatest effect when endogenous estradiol was high. Twelve male (25 ± 1 yr) and 10 female (25 ± 1 yr) participants underwent 30 min of IH. Females were studied in a low (early follicular) and high (late follicular) estradiol state. Preceding and following IH, participants completed two trials [steady-state hypoxia and cold pressor test (CPT)], where forearm blood flow and blood pressure were measured and used to determine forearm vascular conductance (FVC). The FVC response to hypoxia (P= 0.67) and sympathetic activation (P= 0.73) were unchanged following IH in males. There was no effect of IH on hypoxic vasodilation in females, regardless of estradiol state (P= 0.75). In contrast, the vascular response to sympathetic activation was attenuated in females following IH (P= 0.02), independent of estradiol state (P= 0.65). Present data highlight sex-related differences in neurovascular responsiveness following acute IH.NEW & NOTEWORTHYWe examined the effects of acute intermittent hypoxia (AIH) on the vascular response to sympathetic activation and acute hypoxia. Present findings show, despite no effect of AIH on the vascular response to hypoxia, the forearm vasoconstrictor response to acute sympathetic activation is attenuated in females following AIH, independent of estradiol state. These data provide mechanistic understanding of potential benefits of AIH, as well as the impact of biological sex.