Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension
The activation of renin-angiotensin-aldosterine system(RAAS) is one of the main pathogenesis of hypertension. All the components of RAAS are present in the kidneys at higher concentrations compared to plasma levels, and intrarenal formation of angiotensin II (Ang II) is independent of the systemic R...
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The Korean Society of Electrolyte Metabolism
2013
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3950224/ |
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pubmed-39502242014-03-13 Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension Moon, Ju-Young The activation of renin-angiotensin-aldosterine system(RAAS) is one of the main pathogenesis of hypertension. All the components of RAAS are present in the kidneys at higher concentrations compared to plasma levels, and intrarenal formation of angiotensin II (Ang II) is independent of the systemic RAAS. There are some unique features in intrarenal RAAS compared to systemic RAAS. Unlike JG cells where Ang II inhibits renin release via the AngII type 1 (AT1) receptor by negative feedback, in the collecting duct Ang II stimulates renin expression via the AT1 receptor. Upregulated renin produced in the distal nephron may be able to support continued intrarenal Ang II formation leading to amplification or maintenance of the hypertensive state.The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-Angiotensin-(1-7) Ang-(1-7)-Mas receptor axis has an opposing function to that of the ACE-Ang II-AT1 receptor axis.The ACE2 deficiency was associated with an increase in blood pressure, and ACE2 knockout mice have highlighted hypertensive response to Ang II infusion associated with exaggerated accumulation of Ang II in the kidney. Recently, several numbers of patients have been evaluated as the activators of ACE2-Ang-(1-7)-Mas receptor axis, which can be divided into two main classes: aimed to increase the activity of ACE2, and directed to stimulate the Ang-(1-7) receptor Mas. In order to investigate new targets for hypertension and kidney disease, further research on the function of the ACE-Ang-(1-7)-Mas receptor axis is required. The Korean Society of Electrolyte Metabolism 2013-12 2013-12-31 /pmc/articles/PMC3950224/ /pubmed/24627703 http://dx.doi.org/10.5049/EBP.2013.11.2.41 Text en Copyright © 2013 The Korean Society of Electrolyte Metabolism http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Moon, Ju-Young |
| spellingShingle |
Moon, Ju-Young Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| author_facet |
Moon, Ju-Young |
| author_sort |
Moon, Ju-Young |
| title |
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| title_short |
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| title_full |
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| title_fullStr |
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| title_full_unstemmed |
Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension |
| title_sort |
recent update of renin-angiotensin-aldosterone system in the pathogenesis of hypertension |
| description |
The activation of renin-angiotensin-aldosterine system(RAAS) is one of the main pathogenesis of hypertension. All the components of RAAS are present in the kidneys at higher concentrations compared to plasma levels, and intrarenal formation of angiotensin II (Ang II) is independent of the systemic RAAS. There are some unique features in intrarenal RAAS compared to systemic RAAS. Unlike JG cells where Ang II inhibits renin release via the AngII type 1 (AT1) receptor by negative feedback, in the collecting duct Ang II stimulates renin expression via the AT1 receptor. Upregulated renin produced in the distal nephron may be able to support continued intrarenal Ang II formation leading to amplification or maintenance of the hypertensive state.The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-Angiotensin-(1-7) Ang-(1-7)-Mas receptor axis has an opposing function to that of the ACE-Ang II-AT1 receptor axis.The ACE2 deficiency was associated with an increase in blood pressure, and ACE2 knockout mice have highlighted hypertensive response to Ang II infusion associated with exaggerated accumulation of Ang II in the kidney. Recently, several numbers of patients have been evaluated as the activators of ACE2-Ang-(1-7)-Mas receptor axis, which can be divided into two main classes: aimed to increase the activity of ACE2, and directed to stimulate the Ang-(1-7) receptor Mas. In order to investigate new targets for hypertension and kidney disease, further research on the function of the ACE-Ang-(1-7)-Mas receptor axis is required. |
| publisher |
The Korean Society of Electrolyte Metabolism |
| publishDate |
2013 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3950224/ |
| _version_ |
1612066497150058496 |