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The Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor

机译:低肾素高血压表型:遗传和盐皮质激素受体的作用。

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摘要

A substantial proportion of patients with hypertension have a low or suppressed renin. This phenotype of low-renin hypertension (LRH) may be the manifestation of inherited genetic syndromes, acquired somatic mutations, or environmental exposures. Activation of the mineralocorticoid receptor is a common final mechanism for the development of LRH. Classically, the individual causes of LRH have been considered to be rare diseases; however, recent advances suggest that there are milder and “non-classical” variants of many LRH-inducing conditions. In this regard, our understanding of the underlying genetics and mechanisms accounting for LRH, and therefore, potentially the pathogenesis of a large subset of essential hypertension, is evolving. This review will discuss the potential causes of LRH, with a focus on implicated genetic mechanisms, the expanding recognition of non-classical variants of conditions that induce LRH, and the role of the mineralocorticoid receptor in determining this phenotype.
机译:很大一部分高血压患者的肾素水平低或受抑制。低肾素高血压(LRH)的这种表型可能是遗传遗传综合征,获得性体细胞突变或环境暴露的表现。盐皮质激素受体的激活是LRH发展的常见最终机制。传统上,导致LRH的个体原因被认为是罕见疾病。但是,最近的进展表明,许多LRH诱导条件都有较温和且“非经典”的变异。在这方面,我们对导致LRH的潜在遗传学和机制的理解也在不断发展,因此,潜在的大部分原发性高血压的发病机理也在不断发展。这篇综述将讨论LRH的潜在原因,重点在于牵连的遗传机制,诱导LRH的条件的非经典变体的广泛认识以及盐皮质激素受体在确定该表型中的作用。

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