ArticleJournal of the American Society of Nephrology : JASN2011
ETA activation mediates angiotensin II-induced infiltration of renal cortical T cells.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Deletion of the myeloid endothelin-B receptor confers long-term protection from angiotensin II-mediated kidney, eye and vessel injury.Kidney international · 2020Article
- Tauroursodeoxycholic acid (TUDCA) abolishes chronic high salt-induced renal injury and inflammation.Acta physiologica (Oxford, England) · 2019Article
- A novel role for myeloid endothelin-B receptors in hypertension.European heart journal · 2019Article
- ETPhysiological reports · 2018Article
- Attenuation of the Infiltration of Angiotensin II Expressing CD3Frontiers in molecular neuroscience · 2017Article
- Role of the endothelin system in sexual dimorphism in cardiovascular and renal diseases.Life sciences · 2016Review
- Endothelin-1 contributes to the progression of renal injury in sickle cell disease via reactive oxygen species.British journal of pharmacology · 2016Article
- Endothelin antagonists for diabetic and non-diabetic chronic kidney disease.British journal of clinical pharmacology · 2013Review
- Use of ultrasound to assess renal reperfusion and P-selectin expression following unilateral renal ischemia.American journal of physiology. Renal physiology · 2012Article
- Endothelin-1 and the kidney--beyond BP.British journal of pharmacology · 2012Review
- Loss of renal medullary endothelin B receptor function during salt deprivation is regulated by angiotensin II.American journal of physiology. Renal physiology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
T cells and endothelin (ET-1) both contribute to angiotensin II (AngII)-dependent hypertension. To determine whether ET-1, via the ET(A) receptor, facilitates T cell infiltration in the kidney during AngII-dependent hypertension, we measured T cell infiltration in response to four different treatments: saline, AngII infusion, AngII infusion with an ET(A) receptor antagonist, or AngII infusion with triple-antihypertensive therapy. After 14 days, AngII increased both BP and the numbers of CD3(+) and proliferating cells in the kidney. Mice treated concomitantly with the ET(A) receptor antagonist had lower BP and fewer CD3(+) and proliferating cells in the renal cortex. Mice treated with triple therapy had similar reductions in BP but no change in renal cortical CD3(+) cells compared with kidneys from AngII-infused hypertensive mice. In the outer medulla, both the ET(A) receptor antagonist and triple therapy reduced the number of CD3(+) cells and macrophages. Taken together, these data suggest that ET(A) receptor activation in AngII-mediated hypertension increases CD3(+) cells and proliferation in the renal cortex independent of changes in BP, but changes in the number of inflammatory cells in the renal medulla are BP dependent.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.