β-Adrenergic receptors mediate sex differences in vasodilation but not sympathetic-mediated vasoconstriction during hypoxia.

IF 4.1 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Dain W Jacob, Brian Shariffi, Braden J Bond, Natasha G Boyes, Samuel A Martin, Anna M Gonsalves, Jennifer L Harper, Brian P Bostick, Jacqueline K Limberg
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引用次数: 0

Abstract

β-Adrenergic receptors (ARs) mediate a portion of hypoxic vasodilation and blunt sympathetic vasoconstriction at rest. Vascular β-AR sensitivity may be greater in females relative to males; however, their sex-specific role during hypoxia has yet to be examined. We hypothesized β-AR blockade would blunt hypoxic vasodilation and augment sympathetic vasoconstriction during hypoxia, with effects greater in females relative to males. Ten female (26 ± 8 yr, 23 ± 3 kg/m2) and 13 male (28 ± 7 yr, 25 ± 2 kg/m2) adults completed two study visits randomized and blinded to oral placebo or propranolol (β-AR blockade; 1 mg/kg) (NCT05256069). Forearm blood flow (FBF, venous occlusion plethysmography) and blood pressure (BP, finger photoplethysmography) were assessed for 10-min normoxic rest, followed by 5 min of steady-state hypoxia (∼80% [Formula: see text]). Sympathetic activation was achieved via a cold pressor test (CPT) conducted during normoxia and steady-state hypoxia. FBF was normalized for mean BP (forearm vascular conductance, FVC). Absolute (Δ) and relative (%) changes in FVC in response to hypoxia and CPT were calculated. β-AR blockade significantly reduced hypoxic vasodilation in females but not in males (interaction of hypoxia and sex: ΔFVC P = 0.029, %FVC P = 0.030). Sympathetic vasoconstriction was attenuated during hypoxia in females compared with males (main effect of sex: ΔFVC P = 0.005, %FVC P = 0.015), but there was no effect of β-AR blockade in either sex (main effect of drug: ΔFVC P = 0.406; %FVC P = 0.238; interaction of drug and sex: ΔFVC P = 0.619, %FVC P = 0.390). β-Adrenergic receptors mediate hypoxic dilation in females but not in males and do not restrain sympathetic-mediated vasoconstriction during hypoxia in either sex.NEW & NOTEWORTHY β-Adrenergic receptors contribute to hypoxic vasodilation, attenuate sympathetic vasoconstriction at rest, and are more sensitive in females versus males. We hypothesized β-adrenergic receptor blockade would blunt hypoxic vasodilation and augment the sympathetic vasoconstriction during hypoxia, with effects greater in females relative to males. Present data demonstrate β-adrenergic receptors contribute to hypoxic vasodilation in females but do not restrain sympathetic-mediated vasoconstriction during hypoxia in either sex.

β-肾上腺素能受体介导缺氧时血管舒张的性别差异,但不介导交感神经介导的血管收缩。
β-肾上腺素能受体介导部分缺氧血管舒张和静止时钝性交感血管收缩。血管β-AR敏感性在女性中可能高于男性;然而,它们在缺氧时的性别特异性作用还有待研究。我们假设β-AR阻断会减弱缺氧时的血管舒张,增强缺氧时的交感血管收缩,女性的作用比男性更大。方法:10名女性(26±8岁,23±3 kg/m2)和13名男性(28±7岁,25±2 kg/m2)成年人完成了两次随机和盲法的研究访问,口服安慰剂或普萘洛尔(β-AR阻断剂;1毫克/公斤)(NCT05256069)。评估前臂血流(FBF,静脉闭塞体积脉搏图)和血压(BP,手指光体积脉搏图)在10分钟常温休息后,5分钟稳态缺氧(~80% SpO2)。交感神经激活是通过在正常缺氧和稳定缺氧状态下进行的冷压试验(CPT)来实现的。用平均血压(前臂血管传导,FVC)归一化FBF。计算缺氧和CPT对FVC的绝对变化(Δ)和相对变化(%)。结果:β-AR阻断显著降低女性缺氧血管舒张,而男性无(缺氧和性别的相互作用:ΔFVC p=0.029, %FVC p=0.030)。女性在缺氧时交感血管收缩较男性减弱(主要影响因素为性别:ΔFVC p=0.005, %FVC p=0.015),而β-AR阻断在两性中均无影响(主要影响因素为药物:ΔFVC p=0.406;% FVC p = 0.238;性与药物相互作用:ΔFVC p=0.619, %FVC p=0.390)。结论:β-肾上腺素能受体在女性中介导缺氧扩张,而在男性中没有,并且在两性缺氧时不抑制交感神经介导的血管收缩。
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来源期刊
CiteScore
9.60
自引率
10.40%
发文量
202
审稿时长
2-4 weeks
期刊介绍: The American Journal of Physiology-Heart and Circulatory Physiology publishes original investigations, reviews and perspectives on the physiology of the heart, vasculature, and lymphatics. These articles include experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact and integrative animal and organ function to the cellular, subcellular, and molecular levels. The journal embraces new descriptions of these functions and their control systems, as well as their basis in biochemistry, biophysics, genetics, and cell biology. Preference is given to research that provides significant new mechanistic physiological insights that determine the performance of the normal and abnormal heart and circulation.
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