Mineralocorticoids: the secret of muscle reflex dysfunction in hypertension?

Mineralocorticoids: the secret of muscle reflex dysfunction in hypertension?
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盐皮质激素:高血压肌反射功能障碍的秘密?

DOI:
10.1152/ajpheart.00501.2017
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发表时间:
2017
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
Wang,Han-Jun
Wang,Han-Jun
中科院分区:
--
文献类型:
--
作者:
Wang,Han-Jun

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高血压是最常见的人类疾病之一,影响全世界约26%的成年人口(9)。一半的中风和缺血性心脏病事件可归因于高血压(BP)。据报道,高血压患者对运动的心血管反应被夸大,其特征是动脉血压、心率(HR)和交感神经活动增加(1,17,19,27)。考虑到这些患者已经患有高血压,运动引起的交感和升压反应的夸大可能会进一步增加运动期间或运动后立即发生的不良心脑血管事件的风险,包括心肌缺血、心肌梗死、心脏骤停和/或中风。因此,了解运动对高血压心血管反应过度的潜在机制是极其重要的。在过去的十年里,Smith和他的同事们的一系列研究为这一领域做出了重大贡献。总的来说,他们实验室的证据表明,过度活跃的运动加压反射(EPR)是一种起源于骨骼肌的外周神经反射,在几种高血压啮齿动物模型(11,14,15,24)中,运动时心血管反应的异常是原因之一。这种反射的传入臂由代谢敏感纤维(IV,C组)和机械敏感纤维(III组,Aδ)(7,8)组成。2006年,Smith等人(24)首次表明,自发性高血压大鼠(SHR;神经源性高血压模型)通过静态肌肉收缩激活EPR导致的BP和HR增加比正常血压的Wistar-京都大鼠(WKY)更大。此外,Smith和他的同事使用被动肌肉拉伸或后肢动脉内注射辣椒素来优先激活小腿三头肌中的机械感受器或代谢感受器。在这项研究(11)中,机械反射和代谢性反射在SHR中都得到了增强。Mizuno和Smith(14,15)最近的两项研究也检验了在其他高血压模型中表现出增强EPR敏感性的可能性,例如产前编程高血压以及醛固酮和盐负荷引起的高血压。应该注意的是,并不是所有的高血压动物模型都表现出夸大的EPR。例如,O‘Leary和他的同事(18,25)使用了一种肾血管(两肾一夹)高血压犬模型,证明在次极量动态运动中,清醒的两肾一夹狗的血压、心输出量和HR对代谢反射激活的反应与它们的反应相比是迟钝的
HYPERTENSION is one of the most common human disorders, affecting~ 26% of the adult population worldwide (9). Half of all strokes and ischemic heart disease events are attributable to high blood pressure (BP). It has been well reported that the cardiovascular response to exercise is exaggerated in hypertensive patients and characterized by augmented increases in arterial BP, heart rate (HR), and sympathetic nerve activity (1, 17, 19, 27). Considering that these patients already have high BP, the exaggerated exercise-evoked sympathetic and pressor responses could further increase the risk for adverse cardiovascular or cerebrovascular events including myocardial ischemia, myocardial infarction, cardiac arrest, and/or stroke during or immediately after a bout of exercise. Therefore, it is extremely important to understand the potential mechanisms underlying the exaggerated cardiovascular response to exercise in hypertension. In the past decade, a series of studies from Smith and colleagues have made significant contributions to this field. In general, evidence from their laboratory suggests that an overactive exercise pressor reflex (EPR), a peripheral neural reflex originating in skeletal muscle, contributes to this abnormal cardiovascular responsiveness during exercise in several hypertensive rodent models (11, 14, 15, 24). The afferent arm of this reflex is composed of both metabolically sensitive (group IV, C) and mechanically sensitive (group III, Aδ) fibers (7, 8).In 2006, Smith et al.(24) was the first to show that activation of the EPR by static muscle contraction caused greater increases in BP and HR in spontaneous hypertensive rats (SHRs; a neurogenic hypertensive model) than in normotensive Wistar-Kyoto (WKY) rats. Furthermore, Smith and colleagues used either passive muscle stretch or hindlimb intra-arterial administration of capsaicin to preferentially activate mechanoreceptors or metaboreceptors in the triceps surae muscle. In this study (11), both mechano-and metaboreflexes were augmented in SHRs. Two recent studies by Mizuno and Smith (14, 15) also examined the possibility that enhanced EPR sensitivity manifest in other hypertensive models such as prenatal programming of hypertension-and aldosterone and salt loadinginduced hypertension. It should be noted that not all hypertensive animal models exhibit an exaggerated EPR. For example, O’Leary and colleagues (18, 25) used a renovascular (two kidney-one clip) hypertensive canine model to document that BP, cardiac output, and HR responses to metaboreflex activation during submaximal dynamic exercise are blunted in conscious two kidney-one clip dogs compared with their responses
猫背角的 NMDA 受体阻断会减弱对肌肉收缩和伸展的反射性升压反应。
DOI: 10.1152/ajpheart.1996.270.2.h500
发表时间: 1996
期刊: The American journal of physiology.
影响因子: --
作者:
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发表时间: 1983-01-01
期刊: JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
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AOKI, K;SATO, K;YAMAMOTO, M
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DOI: 10.1152/ajpregu.00140.2013
发表时间: 2013
期刊: American journal of physiology. Regulatory, integrative and comparative physiology
影响因子: --
作者:
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