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高血压中的肾髓质。

Renal Medulla in Hypertension.

机构信息

Department of Physiology, Medical College of Wisconsin, Milwaukee (A.W.C., M.M.S., T.K., S.S.).

Medical College of Wisconsin, Milwaukee (A.W.C., M.M.S., T.K., S.S.).

出版信息

Hypertension. 2024 Dec;81(12):2383-2394. doi: 10.1161/HYPERTENSIONAHA.124.21711. Epub 2024 Sep 30.

Abstract

Studies have found that blood flow to the renal medulla is an important determinant of pressure-natriuresis and the long-term regulation of arterial pressure. First, a brief review of methods developed enabling the study of the medullary circulation is presented. Second, studies performed in rats are presented showing medullary blood flow plays a vital role in the pressure-natriuresis relationship and thereby in hypertension. Third, it is shown that chronic reduction of medullary blood flow results in hypertension and that enhancement of medullary blood flow reduces hypertension hereditary models of both salt-sensitive rats and salt-resistant forms of hypertension. The key role that medullary nitric oxide production plays in protecting this region from ischemic injury associated with circulating vasoconstrictor agents and reactive oxygen species is presented. The studies cited are largely the work of my students, research fellows, and colleagues with whom I have performed these studies dating from the late 1980s to more recent years.

摘要

研究发现,肾髓质的血流是压力-利钠作用和动脉血压长期调节的重要决定因素。首先,本文简要回顾了开发这些方法的研究,以研究髓质循环。其次,本文展示了在大鼠中进行的研究,表明髓质血流在压力-利钠作用关系中起着至关重要的作用,从而在高血压中起着至关重要的作用。第三,研究表明,慢性减少髓质血流会导致高血压,而增强髓质血流会降低高血压遗传性模型中盐敏感大鼠和盐抵抗性高血压的高血压。本文介绍了髓质一氧化氮产生在保护该区域免受与循环血管收缩剂和活性氧相关的缺血性损伤方面的关键作用。所引用的研究主要是我从 20 世纪 80 年代末到最近几年与我的学生、研究人员和同事一起进行的这些研究的工作。

相似文献

1
Renal Medulla in Hypertension.高血压中的肾髓质。
Hypertension. 2024 Dec;81(12):2383-2394. doi: 10.1161/HYPERTENSIONAHA.124.21711. Epub 2024 Sep 30.

本文引用的文献

1
Metabolic Responses of Normal Rat Kidneys to a High Salt Intake.正常鼠肾对高盐摄入的代谢反应。
Function (Oxf). 2023 Jun 22;4(5):zqad031. doi: 10.1093/function/zqad031. eCollection 2023.
7
Renal medullary circulation.肾髓质循环。
Compr Physiol. 2012 Jan;2(1):97-140. doi: 10.1002/cphy.c100036.

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