Factors contributing to racial differences in neurogenic orthostatic hypotension.
Factors contributing to racial differences in neurogenic orthostatic hypotension.
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导致神经源性直立性低血压种族差异的因素。
DOI：
10.1007/s10286-021-00775-9
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发表时间：
2021
期刊：
影响因子：
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通讯作者：
Robinson,AustinT
中科院分区：
文献类型：
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作者：
Charkoudian,Nisha;Robinson,AustinT
神经源性直立性低血压(NOH)是阿尔法-突触核病(多系统萎缩、纯自主神经衰竭、帕金森病和路易体痴呆)的特征表现[10，14]。然而，NOH也可以发生在其他疾病中，包括患有糖尿病自主神经病变或罕见的遗传性疾病，如家族性自主神经障碍。Noh可以通过将患者在醒着的大部分时间限制在轮椅上来加剧这些情况的负面后果。在一些压力感受性反射功能障碍的患者中，NOH与仰卧位高血压共存，从而导致单一个体血压谱两端的负面后遗症和风险[14]。近年来，越来越明显的是，我们历史上通过主要在白人男性群体中进行研究，限制了我们对心血管和神经疾病机制的了解[7，8]，限制了我们对发生在不同人群中的疾病的病理生理学的洞察。在这种情况下，我们所说的“种族”主要是一种社会结构[2，22]。然而，同样重要的是要评估在统计上在一个种族群体中可能比在另一个种族群体中更普遍或更不普遍的生物机制，并评估为什么会出现这种情况的潜在原因。在美国和其他国家，动产奴隶制、红线和种族主义的历史至少在一定程度上导致了种族和少数民族面临财富不平等，更有可能经历贫困，生活在不利的社区[2，3，6，15]。这些社会和环境因素通过限制获得健康食品、身体活动的安全空间、环境暴露、睡眠和获得医疗保健的机会来影响心血管疾病风险[11、16、19]。例如，饮食中钾的摄入量存在种族差异，即美国黑人的摄入量比其他种族/民族少[4]。重要的是，低钾饮食与较高的静息血压相关[13]。血压连续体的另一端是Noh，在美国黑人中一直没有得到充分的研究。在这一期的临床自主研究中，Giza和他的同事对非西班牙裔黑人男性的Noh提供了新的生物学见解[12]。研究人员研究了9名患有NOH的非西班牙裔黑人个体的心血管和神经体液数据，并与非西班牙裔白人NOH个体和8名非西班牙裔白人健康对照组进行了比较。他们报告说，许多与NOH相关的变量，包括血液动力学和直立姿势下血浆去甲肾上腺素的变化，在非西班牙裔黑人和非西班牙裔白人NOH患者中是相似的。然而，非西班牙裔黑人和非西班牙裔白人患者在血浆肾素活性和对直立姿势的醛固酮反应方面存在显著差异。而非西班牙裔白人患者和对照组在直立的非西班牙裔黑人患者只有非常微小的变化时，血浆肾素活性和醛固酮显著增加，这些都没有统计学意义[12]。在容量调节方面，有趣的是，温纳和他的同事还报告说，与非西班牙裔白人个体相比，健康的非西班牙裔黑人的血浆肾素活性和醛固酮反应对钠负荷的反应减弱(减少)[21]。
Neurogenic orthostatic hypotension (nOH) is a characteristic manifestation of the alpha-synucleinopathies (multiple system atrophy, pure autonomic failure, Parkinson disease and dementia with Lewy bodies)[10, 14]. However, nOH can occur in other disorders as well, including people with diabetic autonomic neuropathy or rare genetic disorders like familial dysautonomia. nOH can exacerbate the negative consequences of any of these conditions by confining the individual to a wheelchair for most of their waking hours. In some patients with baroreflex dysfunction, nOH coexists with supine hypertension, thus resulting in the negative sequelae and risks of both ends of the blood pressure spectrum in a single individual [14]. It has become increasingly clear in recent years that we have historically limited our understanding of mechanisms of cardiovascular and neurological diseases by conducting research primarily in groups of white men [7, 8], limiting our insight into the pathophysiology of diseases that occur in a diverse population. In this context, what we call “race” is primarily a social construct [2, 22]. However, it is also important to evaluate biological mechanisms that might be statistically more or less prevalent in one racial group than another, and to evaluate potential reasons why this might be the case. In the United States and other countries, a history of chattel slavery, redlining, and racism have, at least in part, contributed to racial and ethnic minorities facing wealth inequality and being more likely to experience poverty and live in disadvantaged neighborhoods [2, 3, 6, 15]. These social and environmental factors influence cardiovascular disease risk by limiting access to healthful foods, safe spaces for physical activity, environmental exposures, sleep, and access to healthcare [11, 16, 19]. For example, there are racial disparities in dietary potassium intake, namely Black Americans consume less than other racial/ethnic groups [4]. Importantly, lower dietary potassium is associated with higher resting blood pressure [13]. At the other end of the blood pressure continuum is nOH, which has been understudied in Black Americans.In this issue of Clinical Autonomic Research, Giza and colleagues provide novel biological insight into nOH in non-Hispanic Black men [12]. The investigators studied cardiovascular and neurohumoral data in nine non-Hispanic Black individuals with nOH and compared to non-Hispanic White individuals with nOH and to a group of 8 non-Hispanic White healthy control subjects. They report that many of the variables relevant to nOH, including hemodynamic and plasma norepinephrine changes with upright posture, were similar in non-Hispanic Black and non-Hispanic White patients with nOH. However, there were marked differences between non-Hispanic Black and non-Hispanic White patients in terms of plasma renin activity and aldosterone responses to upright posture. Whereas non-Hispanic White patients and controls had marked increases in plasma renin activity and aldosterone when upright, non-Hispanic Black patients had only very small changes, and these were not statistically significant [12]. In terms of volume regulation, it is intriguing that Wenner and colleagues also reported a diminished responsiveness (reduction) in plasma renin activity and aldosterone response to sodium loading in healthy non-Hispanic Black, compared to non-Hispanic White, individuals [21].