ACE2 and angiotensin-(1-7) in hypertensive renal disease
Electrolyte and Blood Pressure, ISSN: 1738-5997, Vol: 9, Issue: 2, Page: 41-44
2011
- 14Citations
- 25Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations14
- Citation Indexes14
- 14
- CrossRef9
- Captures25
- Readers25
- 25
- Mentions1
- News Mentions1
- News1
Most Recent News
Renal Transplant Injury and the Renin-Angiotensin System in Kids (RETASK); RETASK
STUDY INFORMATION OFFICIAL TITLE: Renal Transplant Injury and the Renin-Angiotensin System in Kids (RETASK) CURRENT STATUS: Completed STUDY TYPE: Observational SPONSOR AGENCY:Wake Forest University Health
Review Description
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-Anglotensln II (Ang II)-Angiotensin type 1 (AT1) receptor axis. Ang-(1-7) is present in the kidneys at concentrations comparable to those of Ang II and is associated with vasodilation, modulation of sodium and water transport, and stimulation of nitric oxide (NO) synthase. Ang-(1-7) also acts as a physiological antagonist of Ang II by counterbalancing the Ang II-mediated intracellular signaling pathway. In a hypertensive model, increased ACE and decreased ACE2 along with a higher ACE/ACE2 ratio in hypertensive kidneys appeared to favor Ang II generation, leading to hypertensive renal damage. In addition, the administration of a selective Ang-(1-7) receptor blocker or an ACE2 inhibitor was associated with worsening of hypertension and renal function. Ang-(1-7)-mediated increases in renal blood flow were abolished by blockade of the Mas receptor and by inhibition of prostaglandin release and NO in spontaneously hypertensive rats and in Wistar-Kyoto controls. Further research on the function of the ACE2-Ang-(1-7)-Mas receptor axis could lead to a novel target for inhibiting kidney disease progression. Copyright © 2011 The Korean Society of Electrolyte Metabolism.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84869190843&origin=inward; http://dx.doi.org/10.5049/ebp.2011.9.2.41; http://www.ncbi.nlm.nih.gov/pubmed/22438854; https://enbpr.org/DOIx.php?id=10.5049/EBP.2011.9.2.41; https://synapse.koreamed.org/DOIx.php?id=10.5049/EBP.2011.9.2.41; http://synapse.koreamed.org/DOIx.php?id=10.5049/EBP.2011.9.2.41
The Korean Society of Electrolyte Metabolism
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