Williams Auni C, Alexander Lacy M
Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park (A.C.W., L.M.A.).
Center for Healthy Aging, The Pennsylvania State University, University Park (L.M.A.).
Hypertension. 2025 Aug 1. doi: 10.1161/HYPERTENSIONAHA.125.25089.
Endometriosis is a risk factor for cardiovascular disease. COX (Cyclooxygenase) is upregulated in endometriotic lesions, potentially exaggerating pressor reflexes, a major risk factor for adverse cardiovascular events. The purpose of this study was to determine whether women with endometriosis demonstrate exaggerated pressor responses. We hypothesized that women with endometriosis would show exaggerated BP compared with healthy women during handgrip exercise and cold pressor testing (CPT).
In a single-blind, randomized, crossover design, women with (Endo ; n=11) and without (HC; n=9) endometriosis underwent a CPT and handgrip with postexercise ischemia following aspirin (a nonselective COX inhibitor; 650 mg) or placebo. Blood pressure was continuously monitored during baseline (5 minutes) and hand submersion (3 minutes; 4-8 °C) during CPT, and during baseline (5 minutes), 30% maximal voluntary contraction handgrip (2 minutes), and postexercise ischemia (3 minutes) for handgrip with postexercise ischemia.
Women with endometriosis demonstrated attenuated pressor responses to CPT (∆MAP Endo 21±16 versus HC 34±20 mm Hg; <0.01) and handgrip with postexercise ischemia (handgrip/postexercise ischemia: ΔMAP Endo=12±13/13±10 mm Hg, HC=24±14/20±8 mm Hg; <0.01). There was no effect of aspirin on blood pressure response to either CPT or handgrip with postexercise ischemia.
Compared with age-matched HC, women with endometriosis demonstrate lower increases in blood pressure in response to cold exposure and exercise. Aspirin, a COX inhibitor, had no impact on these responses. Collectively, these results suggest that women with endometriosis demonstrate altered central integration and attenuated sympathetic outflow and end-organ responsiveness.
子宫内膜异位症是心血管疾病的一个危险因素。环氧化酶(COX)在子宫内膜异位症病灶中上调,可能会加剧压力反射,而压力反射是不良心血管事件的一个主要危险因素。本研究的目的是确定患有子宫内膜异位症的女性是否表现出夸张的压力反应。我们假设,与健康女性相比,患有子宫内膜异位症的女性在握力运动和冷加压试验(CPT)期间会表现出更高的血压。
在一项单盲、随机、交叉设计中,患有(子宫内膜异位症组;n = 11)和未患有(健康对照组;n = 9)子宫内膜异位症的女性在服用阿司匹林(一种非选择性COX抑制剂;650 mg)或安慰剂后进行了CPT和握力运动及运动后缺血试验。在CPT期间的基线(5分钟)和手部浸入(3分钟;4 - 8°C)期间,以及在握力运动及运动后缺血试验的基线(5分钟)、30%最大自主收缩握力(2分钟)和运动后缺血(3分钟)期间持续监测血压。
患有子宫内膜异位症的女性对CPT的压力反应减弱(平均动脉压变化:子宫内膜异位症组21±16,健康对照组34±20 mmHg;<0.01),对握力运动及运动后缺血的压力反应也减弱(握力运动/运动后缺血:平均动脉压变化,子宫内膜异位症组=12±13/13±10 mmHg,健康对照组=24±14/20±8 mmHg;<0.01)。阿司匹林对CPT或握力运动及运动后缺血的血压反应均无影响。
与年龄匹配的健康对照组相比,患有子宫内膜异位症的女性对冷暴露和运动的血压升高反应较低。COX抑制剂阿司匹林对这些反应没有影响。总体而言,这些结果表明,患有子宫内膜异位症的女性表现出中枢整合改变、交感神经输出减弱和终末器官反应性降低。