Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion

Abstract We investigate whether suppressing the activation of the angiotensin II type 1a receptor (AT1a) can ameliorate severe chronic tubulointerstitial damage (TID) after renal ischemia reperfusion (IR) using AT1a knockout homozygous (AT1a−/−) male mice. To induce severe chronic TID after renal IR...

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Autores principales:	Yoko Fujita, Daisuke Ichikawa, Takeshi Sugaya, Keiichi Ohata, Jun Tanabe, Kazuho Inoue, Seiko Hoshino, Tatsuru Togo, Minoru Watanabe, Kenjiro Kimura, Yugo Shibagaki, Atsuko Kamijo-Ikemori
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/18eb73f97dd64954b6068a75ce099b1d
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spelling	oai:doaj.org-article:18eb73f97dd64954b6068a75ce099b1d2021-12-02T14:12:09ZAngiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion10.1038/s41598-020-80209-02045-2322https://doaj.org/article/18eb73f97dd64954b6068a75ce099b1d2021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-80209-0https://doaj.org/toc/2045-2322Abstract We investigate whether suppressing the activation of the angiotensin II type 1a receptor (AT1a) can ameliorate severe chronic tubulointerstitial damage (TID) after renal ischemia reperfusion (IR) using AT1a knockout homozygous (AT1a−/−) male mice. To induce severe chronic TID after renal IR, unilateral renal ischemia was performed via clamping of the right renal pedicle in both AT1a−/− and wild-type (AT1a+/+) mice for 45 min. While marked renal atrophy and severe TID at 70 days postischemia was induced in the AT1a+/+ mice, such a development was not provoked in the AT1a−/− mice. Although the AT1a+/+ mice were administered hydralazine to maintain the same systolic blood pressure (SBP) levels as the AT1a−/− mice with lower SBP levels, hydralazine did not reproduce the renoprotective effects observed in the AT1a−/− mice. Acute tubular injury at 3 days postischemia was similar between the AT1a−/− mice and the AT1a+/+ mice. From our investigations using IR kidneys at 3, 14, and 28 days postischemia, the multiple molecular mechanisms may be related to prevention of severe chronic TID postischemia in the AT1a−/− mice. In conclusion, inactivation of the AT1 receptor may be useful in preventing the transition of acute kidney injury to chronic kidney disease.Yoko FujitaDaisuke IchikawaTakeshi SugayaKeiichi OhataJun TanabeKazuho InoueSeiko HoshinoTatsuru TogoMinoru WatanabeKenjiro KimuraYugo ShibagakiAtsuko Kamijo-IkemoriNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yoko Fujita Daisuke Ichikawa Takeshi Sugaya Keiichi Ohata Jun Tanabe Kazuho Inoue Seiko Hoshino Tatsuru Togo Minoru Watanabe Kenjiro Kimura Yugo Shibagaki Atsuko Kamijo-Ikemori Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
description	Abstract We investigate whether suppressing the activation of the angiotensin II type 1a receptor (AT1a) can ameliorate severe chronic tubulointerstitial damage (TID) after renal ischemia reperfusion (IR) using AT1a knockout homozygous (AT1a−/−) male mice. To induce severe chronic TID after renal IR, unilateral renal ischemia was performed via clamping of the right renal pedicle in both AT1a−/− and wild-type (AT1a+/+) mice for 45 min. While marked renal atrophy and severe TID at 70 days postischemia was induced in the AT1a+/+ mice, such a development was not provoked in the AT1a−/− mice. Although the AT1a+/+ mice were administered hydralazine to maintain the same systolic blood pressure (SBP) levels as the AT1a−/− mice with lower SBP levels, hydralazine did not reproduce the renoprotective effects observed in the AT1a−/− mice. Acute tubular injury at 3 days postischemia was similar between the AT1a−/− mice and the AT1a+/+ mice. From our investigations using IR kidneys at 3, 14, and 28 days postischemia, the multiple molecular mechanisms may be related to prevention of severe chronic TID postischemia in the AT1a−/− mice. In conclusion, inactivation of the AT1 receptor may be useful in preventing the transition of acute kidney injury to chronic kidney disease.
format	article
author	Yoko Fujita Daisuke Ichikawa Takeshi Sugaya Keiichi Ohata Jun Tanabe Kazuho Inoue Seiko Hoshino Tatsuru Togo Minoru Watanabe Kenjiro Kimura Yugo Shibagaki Atsuko Kamijo-Ikemori
author_facet	Yoko Fujita Daisuke Ichikawa Takeshi Sugaya Keiichi Ohata Jun Tanabe Kazuho Inoue Seiko Hoshino Tatsuru Togo Minoru Watanabe Kenjiro Kimura Yugo Shibagaki Atsuko Kamijo-Ikemori
author_sort	Yoko Fujita
title	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
title_short	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
title_full	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
title_fullStr	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
title_full_unstemmed	Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
title_sort	angiotensin ii type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/18eb73f97dd64954b6068a75ce099b1d
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Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion

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