The angiotensin II type 2 receptor in renal disease
Suppression of angiotensin II formation by angiotensin-converting enzyme inhibitors or blockade of the angiotensin II receptor by angiotensin receptor blockers is a powerful therapeutic strategy to slow the progression of renal disease. However, angiotensin-converting enzyme inhibitors and angiotens...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publications
2010-03-01
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| Series: | Journal of the Renin-Angiotensin-Aldosterone System |
| Online Access: | https://doi.org/10.1177/1470320309347787 |
| _version_ | 1797285377949564928 |
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| author | Ulrich Otto Wenzel Christian Krebs Ralf Benndorf |
| author_facet | Ulrich Otto Wenzel Christian Krebs Ralf Benndorf |
| author_sort | Ulrich Otto Wenzel |
| collection | DOAJ |
| description | Suppression of angiotensin II formation by angiotensin-converting enzyme inhibitors or blockade of the angiotensin II receptor by angiotensin receptor blockers is a powerful therapeutic strategy to slow the progression of renal disease. However, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers provide only imperfect protection against the progression of chronic kidney disease to end-stage renal failure. Hence, innovative approaches are needed to keep patients with chronic kidney disease off dialysis. Angiotensin II activates at least two receptors, namely the angiotensin II type 1 (AT 1 ) and angiotensin II type 2 (AT 2 ) receptors. The majority of the effects of angiotensin II, such as vasoconstriction, inflammation, and matrix deposition, are mediated via the AT 1 receptor. It is thought that the AT 2 receptor counteracts these effects and plays a role in nephroprotection. However, recent data support the notion that the AT 2 receptor transduces pro-inflammatory effects and promotes fibrosis and hypertrophy. Therefore, the question of whether stimulation of the AT 2 receptor could represent a silver bullet for the treatment of chronic kidney disease or may, on the contrary, exert detrimental effects on renal physiology remains unresolved. Recent data from AT 2 receptor-knockout mice demonstrate that the loss of AT 2 receptor signalling is associated with increased renal injury and mortality in chronic kidney disease. This raises the expectation that pharmacological stimulation of the AT 2 receptor may positively influence renal pathologies. However, further research is needed to explore the question whether AT 2 receptor stimulation may represent a new therapeutic strategy for the treatment of chronic kidney disease. |
| first_indexed | 2024-03-07T18:02:18Z |
| format | Article |
| id | doaj.art-1056c52b7fdd40beae8f88ac90969280 |
| institution | Directory Open Access Journal |
| issn | 1470-3203 |
| language | English |
| last_indexed | 2024-03-07T18:02:18Z |
| publishDate | 2010-03-01 |
| publisher | SAGE Publications |
| record_format | Article |
| series | Journal of the Renin-Angiotensin-Aldosterone System |
| spelling | doaj.art-1056c52b7fdd40beae8f88ac909692802024-03-02T10:24:28ZengSAGE PublicationsJournal of the Renin-Angiotensin-Aldosterone System1470-32032010-03-011110.1177/1470320309347787The angiotensin II type 2 receptor in renal diseaseUlrich Otto WenzelChristian KrebsRalf BenndorfSuppression of angiotensin II formation by angiotensin-converting enzyme inhibitors or blockade of the angiotensin II receptor by angiotensin receptor blockers is a powerful therapeutic strategy to slow the progression of renal disease. However, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers provide only imperfect protection against the progression of chronic kidney disease to end-stage renal failure. Hence, innovative approaches are needed to keep patients with chronic kidney disease off dialysis. Angiotensin II activates at least two receptors, namely the angiotensin II type 1 (AT 1 ) and angiotensin II type 2 (AT 2 ) receptors. The majority of the effects of angiotensin II, such as vasoconstriction, inflammation, and matrix deposition, are mediated via the AT 1 receptor. It is thought that the AT 2 receptor counteracts these effects and plays a role in nephroprotection. However, recent data support the notion that the AT 2 receptor transduces pro-inflammatory effects and promotes fibrosis and hypertrophy. Therefore, the question of whether stimulation of the AT 2 receptor could represent a silver bullet for the treatment of chronic kidney disease or may, on the contrary, exert detrimental effects on renal physiology remains unresolved. Recent data from AT 2 receptor-knockout mice demonstrate that the loss of AT 2 receptor signalling is associated with increased renal injury and mortality in chronic kidney disease. This raises the expectation that pharmacological stimulation of the AT 2 receptor may positively influence renal pathologies. However, further research is needed to explore the question whether AT 2 receptor stimulation may represent a new therapeutic strategy for the treatment of chronic kidney disease.https://doi.org/10.1177/1470320309347787 |
| spellingShingle | Ulrich Otto Wenzel Christian Krebs Ralf Benndorf The angiotensin II type 2 receptor in renal disease Journal of the Renin-Angiotensin-Aldosterone System |
| title | The angiotensin II type 2 receptor in renal disease |
| title_full | The angiotensin II type 2 receptor in renal disease |
| title_fullStr | The angiotensin II type 2 receptor in renal disease |
| title_full_unstemmed | The angiotensin II type 2 receptor in renal disease |
| title_short | The angiotensin II type 2 receptor in renal disease |
| title_sort | angiotensin ii type 2 receptor in renal disease |
| url | https://doi.org/10.1177/1470320309347787 |
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