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:
影响因子:
--
通讯作者:
Wang,Han-Jun
中科院分区:
文献类型:
--
作者:
Wang,Han-Jun
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
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