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高血压血管重塑的病理生理学

Pathophysiology of vascular remodeling in hypertension.

作者信息

Renna Nicolás F, de Las Heras Natalia, Miatello Roberto M

机构信息

Department of Pathology, School of Medicine, National University of Cuyo, Avenida Libertador 80, Centro Universitario, 5500 Mendoza, Argentina ; Institute of Experimental Medicine and Biology of Cuyo (IMBECU), CONICET, Mendoza, Argentina.

出版信息

Int J Hypertens. 2013;2013:808353. doi: 10.1155/2013/808353. Epub 2013 Jul 22.

DOI:10.1155/2013/808353
PMID:23970958
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3736482/
Abstract

Vascular remodeling refers to alterations in the structure of resistance vessels contributing to elevated systemic vascular resistance in hypertension. We start with some historical aspects, underscoring the importance of Glagov's contribution. We then move to some basic concepts on the biomechanics of blood vessels and explain the definitions proposed by Mulvany for specific forms of remodeling, especially inward eutrophic and inward hypertrophic. The available evidence for the existence of remodeled resistance vessels in hypertension comes next, with relatively more weight given to human, in comparison with animal data. Mechanisms are discussed. The impact of antihypertensive drug treatment on remodeling is described, again with emphasis on human data. Some details are given on the three mechanisms to date which point to remodeling resistance arteries as an independent predictor of cardiovascular risk in hypertensive patients. We terminate by considering the potential role of remodeling in the pathogenesis of endorgan damage and in the perpetuation of hypertension.

摘要

血管重塑是指阻力血管结构的改变,这会导致高血压患者全身血管阻力升高。我们首先介绍一些历史方面的内容,强调格拉戈夫贡献的重要性。然后我们转向血管生物力学的一些基本概念,并解释马尔瓦尼提出的特定重塑形式的定义,特别是内向性营养性和内向性肥厚性重塑。接下来是高血压中存在重塑阻力血管的现有证据,与动物数据相比,相对更重视人体数据。讨论了相关机制。描述了降压药物治疗对重塑的影响,同样强调人体数据。详细介绍了迄今为止的三种机制,这些机制表明重塑的阻力动脉是高血压患者心血管风险的独立预测因素。我们最后考虑重塑在终末器官损伤发病机制和高血压持续存在中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/748fba72bb32/IJHT2013-808353.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/a4e7ddb20884/IJHT2013-808353.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/6190de20dfa5/IJHT2013-808353.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/748fba72bb32/IJHT2013-808353.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/a4e7ddb20884/IJHT2013-808353.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/6190de20dfa5/IJHT2013-808353.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b8a/3736482/748fba72bb32/IJHT2013-808353.003.jpg

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