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本文引用的文献

1
Sestrin2 decreases renal oxidative stress, lowers blood pressure, and mediates dopamine D2 receptor-induced inhibition of reactive oxygen species production.Sestrin2可降低肾脏氧化应激,降低血压,并介导多巴胺D2受体诱导的活性氧生成抑制。
Hypertension. 2014 Oct;64(4):825-32. doi: 10.1161/HYPERTENSIONAHA.114.03840. Epub 2014 Jul 14.
2
First D1-like receptor PET imaging of the rat and primate kidney: implications for human disease monitoring.大鼠和灵长类动物肾脏的首次D1样受体正电子发射断层显像:对人类疾病监测的意义
Am J Physiol Renal Physiol. 2014 Jul 1;307(1):F116-21. doi: 10.1152/ajprenal.00111.2014. Epub 2014 May 7.
3
Roles of dopamine receptor on chemosensory and mechanosensory primary cilia in renal epithelial cells.多巴胺受体在肾脏上皮细胞的化学感觉和机械感觉初级纤毛中的作用。
Front Physiol. 2014 Feb 26;5:72. doi: 10.3389/fphys.2014.00072. eCollection 2014.
4
The cooperative roles of the dopamine receptors, D1R and D5R, on the regulation of renal sodium transport.多巴胺受体D1R和D5R在肾钠转运调节中的协同作用。
Kidney Int. 2014 Jul;86(1):118-26. doi: 10.1038/ki.2014.5. Epub 2014 Feb 19.
5
Regulation of renalase expression by D5 dopamine receptors in rat renal proximal tubule cells.多巴胺 D5 受体调节大鼠肾近曲小管细胞肾酶的表达。
Am J Physiol Renal Physiol. 2014 Mar 15;306(6):F588-96. doi: 10.1152/ajprenal.00196.2013. Epub 2014 Feb 5.
6
Single-nucleotide polymorphisms of the dopamine D2 receptor increase inflammation and fibrosis in human renal proximal tubule cells.多巴胺 D2 受体单核苷酸多态性增加人肾近端肾小管细胞的炎症和纤维化。
Hypertension. 2014 Mar;63(3):e74-80. doi: 10.1161/HYPERTENSIONAHA.113.02569. Epub 2013 Dec 30.
7
Dopamine D3 receptor inhibits the ubiquitin-specific peptidase 48 to promote NHE3 degradation.多巴胺 D3 受体抑制泛素特异性肽酶 48 以促进 NHE3 的降解。
FASEB J. 2014 Mar;28(3):1422-34. doi: 10.1096/fj.13-243840. Epub 2013 Dec 5.
8
Role of epoxyeicosatrienoic acids (EETs) in mediation of dopamine's effects in the kidney.环氧二十碳三烯酸(EETs)在介导多巴胺对肾脏作用中的作用。
Am J Physiol Renal Physiol. 2013 Dec 15;305(12):F1680-6. doi: 10.1152/ajprenal.00409.2013. Epub 2013 Oct 23.
9
Renalase in hypertension and kidney disease.肾酶与高血压及肾脏疾病。
Nephrol Dial Transplant. 2014 Jan;29(1):22-8. doi: 10.1093/ndt/gft083. Epub 2013 Oct 17.
10
Direct inhibition of basolateral Kir4.1/5.1 and Kir4.1 channels in the cortical collecting duct by dopamine.多巴胺对皮质集合管基底外侧 Kir4.1/5.1 和 Kir4.1 通道的直接抑制作用。
Am J Physiol Renal Physiol. 2013 Nov 1;305(9):F1277-87. doi: 10.1152/ajprenal.00363.2013. Epub 2013 Aug 28.

肾内多巴胺的降压机制。

Antihypertensive mechanisms of intra-renal dopamine.

作者信息

Zhang Ming-Zhi, Harris Raymond C

机构信息

Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA.

出版信息

Curr Opin Nephrol Hypertens. 2015 Mar;24(2):117-22. doi: 10.1097/MNH.0000000000000104.

DOI:10.1097/MNH.0000000000000104
PMID:25594544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4651846/
Abstract

PURPOSE OF REVIEW

This review will highlight recent findings concerning the regulation and signalling of the intrarenal dopaminergic system and the emerging evidence for its importance in blood pressure regulation.

RECENT FINDINGS

There is an increasing evidence that the intrarenal dopaminergic system plays an important role in the regulation of blood pressure, and defects in dopamine signalling appear to be involved in the development of hypertension. Recent experimental models have definitively demonstrated that abnormalities in intrarenal dopamine production or receptor signalling can predispose to salt-sensitive hypertension and a dysregulated renin-angiotensin system. There are also new results indicating the importance of dopamine receptor mediated regulation of salt and water homeostasis along the nephron, and new studies indicating the role that the intrarenal dopaminergic system plays to mitigate the production of reactive oxygen species and progression of chronic renal disease.

SUMMARY

New studies underscore the importance of the intrarenal dopaminergic system in the regulation of renal function and indicate how alterations in dopamine production or signalling may underlie the development of hypertension and kidney injury.

摘要

综述目的

本综述将重点介绍有关肾内多巴胺能系统调节和信号传导的最新研究结果,以及其在血压调节中重要性的新证据。

最新发现

越来越多的证据表明,肾内多巴胺能系统在血压调节中起重要作用,多巴胺信号传导缺陷似乎与高血压的发生有关。最近的实验模型已明确证明,肾内多巴胺生成或受体信号传导异常可导致盐敏感性高血压和肾素 - 血管紧张素系统失调。也有新结果表明多巴胺受体介导的沿肾单位调节盐和水平衡的重要性,以及新研究表明肾内多巴胺能系统在减轻活性氧生成和慢性肾病进展方面的作用。

总结

新研究强调了肾内多巴胺能系统在肾功能调节中的重要性,并指出多巴胺生成或信号传导的改变可能是高血压和肾损伤发生的基础。