Polycystic ovary syndrome potentiates blood pressure and vascular responses to the cold pressor test.

IF 3.3 3区 医学 Q1 PHYSIOLOGY
Journal of applied physiology Pub Date : 2025-02-01 Epub Date: 2024-12-11 DOI:10.1152/japplphysiol.00697.2024
Danielle E Berbrier, Yasmine Coovadia, Divine Malenda, Charlotte W Usselman
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引用次数: 0

Abstract

Polycystic ovary syndrome (PCOS) predisposes women to cardiovascular diseases. Blood pressure (BP) responses to the cold pressor test (CPT) predict future cardiovascular risk but have yet to be characterized in PCOS. Therefore, we compared BP responses to the CPT between females with PCOS [n = 10; age: 22 ± 3 yr, body mass index (BMI): 23.9 ± 3 kg/m2] and healthy controls (CTRL; n = 10; age: 22 ± 2 yr, BMI: 22.1 ± 2 kg/m2). BP (finger photoplethysmography calibrated to manual sphygmomanometry-derived values), femoral blood flow (duplex ultrasound), and vascular resistance [FVR; mean arterial pressure (MAP)/blood flow] were measured continuously at baseline and across a 3-min hand CPT. Venous blood samples were used to quantify the free androgen index (FAI; total testosterone/sex hormone binding globulin × 100). Baseline MAP was not different between PCOS and CTRL (87 ± 7 vs. 82 ± 11 mmHg, respectively; P = 0.25), nor was systolic BP (SBP; 109 ± 9 vs. 106 ± 7 mmHg; P = 0.42). Across the CPT, MAP and SBP were higher in PCOS than CTRL (main effects of group, both P < 0.05). Peak CPT induced increases in MAP (+12 ± 5 vs. +7 ± 4 mmHg; P = 0.04) and corresponding changes in SBP (+13 ± 7 vs. +7 ± 3 mmHg; P = 0.04) and FVR (+0.17 ± 0.08 vs. +0.02 ± 0.13 mmHg/mL/min; P = 0.01) were larger in PCOS than CTRL. Within-group regressions indicated that FAI was positively associated with relative increases in peak MAP (R2 = 0.72, P < 0.01) and corresponding changes in FVR (R2 = 0.83, P < 0.01) in females with PCOS but not in CTRL (MAP: R2 = 0.03, P = 0.62; FVR: R2 = 0.12, P = 0.41). Young, lean females with PCOS demonstrate exaggerated BP and vascular responses to the CPT that may be indicative of elevated cardiovascular risk mediated in part by the detrimental effects of elevated androgens.NEW & NOTEWORTHY Young, lean, and otherwise healthy females with polycystic ovary syndrome (PCOS) demonstrated exaggerated blood pressure responses to the cold pressor test (CPT) relative to controls. CPT responses were associated with bioavailable androgens, suggesting that hyperandrogenism contributes to exaggerated responses to the CPT in PCOS. Given associations between CPT responsiveness and the subsequent development of hypertension, these findings add to mounting evidence for increased cardiovascular risk even in lean females with PCOS.

多囊卵巢综合征增强血压和血管反应冷压试验。
多囊卵巢综合征(PCOS)使妇女易患心血管疾病。冷压试验(CPT)的血压(BP)反应预测未来心血管风险,但尚未表征PCOS。因此,我们比较了PCOS女性患者对CPT的血压反应(n=10;年龄:22±3岁,体质指数(BMI): 23.9±3 kg/m2,健康对照组(CTRL;n = 10;22±2yr, 22.1±2kg /m2)。BP(手指光波脉搏图校准到手动血压计衍生值),股血流量(双工超声)和血管阻力(FVR;在基线和3分钟手部CPT期间连续测量平均动脉压(MAP) /血流量。静脉血样本用于定量游离雄激素指数(FAI);总睾酮/性激素结合球蛋白*100)。PCOS和CTRL组的基线MAP无差异(分别为87±7 vs 82±11mmHg, P=0.25),收缩压(SBP;109±9比106±7mmHg, P=0.42)。PCOS组CPT、MAP和SBP均高于对照组(两组均有主要影响),PCOS组CPT诱导的MAP峰值升高(+12±5 vs +7±4mmHg, P=0.04),相应的SBP变化(+13±7 vs +7±3mmHg, P=0.04)和FVR(+0.17±0.08 vs +0.02±0.13mmHg/mL/min, P=0.01)均高于对照组。组内回归分析显示,FAI与PCOS女性患者MAP峰相对升高(R2=0.72, P)和FVR相应变化(R2=0.83, P)呈正相关,而与CTRL组无相关(MAP: R2=0.03, P=0.62;Fvr: r2 =0.12, p =0.41)。年轻、瘦削的女性多囊卵巢综合征患者对CPT的血压和血管反应过高,这可能表明雄激素升高的有害影响部分介导了心血管风险升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.00
自引率
9.10%
发文量
296
审稿时长
2-4 weeks
期刊介绍: The Journal of Applied Physiology publishes the highest quality original research and reviews that examine novel adaptive and integrative physiological mechanisms in humans and animals that advance the field. The journal encourages the submission of manuscripts that examine the acute and adaptive responses of various organs, tissues, cells and/or molecular pathways to environmental, physiological and/or pathophysiological stressors. As an applied physiology journal, topics of interest are not limited to a particular organ system. The journal, therefore, considers a wide array of integrative and translational research topics examining the mechanisms involved in disease processes and mitigation strategies, as well as the promotion of health and well-being throughout the lifespan. Priority is given to manuscripts that provide mechanistic insight deemed to exert an impact on the field.
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