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An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model.
Kidney Int. 2017 05; 91(5):1115-1125.KI

Abstract

Angiotensin II type 1 receptor-associated protein (ATRAP) promotes AT1R internalization along with suppression of hyperactivation of tissue AT1R signaling. Here, we provide evidence that renal ATRAP plays a critical role in suppressing hypertension in a mouse remnant kidney model of chronic kidney disease. The effect of 5/6 nephrectomy on endogenous ATRAP expression was examined in the kidney of C57BL/6 and 129/Sv mice. While 129/Sv mice with a remnant kidney showed decreased renal ATRAP expression and developed hypertension, C57BL/6 mice exhibited increased renal ATRAP expression and resistance to progressive hypertension. Consequently, we hypothesized that downregulation of renal ATRAP expression is involved in pathogenesis of hypertension in the remnant kidney model of chronic kidney disease. Interestingly, 5/6 nephrectomy in ATRAP-knockout mice on the hypertension-resistant C57BL/6 background caused hypertension with increased plasma volume. Moreover, in knockout compared to wild-type C57BL/6 mice after 5/6 nephrectomy, renal expression of the epithelial sodium channel α-subunit and tumor necrosis factor-α was significantly enhanced, concomitant with increased plasma membrane angiotensin II type 1 receptor in the kidneys. Thus, renal ATRAP downregulation is involved in the onset and progression of blood pressure elevation caused by renal mass reduction, and implicates ATRAP as a therapeutic target for hypertension in chronic kidney disease.

Authors+Show Affiliations

Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan. Electronic address: hiro1234@yokohama-cu.ac.jp.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Pharmacology, Kagawa University School of Medicine, Kagawa, Japan.Department of Molecular Biology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan. Electronic address: tamukou@med.yokohama-cu.ac.jp.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28081856

Citation

Kobayashi, Ryu, et al. "An Angiotensin II Type 1 Receptor Binding Molecule Has a Critical Role in Hypertension in a Chronic Kidney Disease Model." Kidney International, vol. 91, no. 5, 2017, pp. 1115-1125.
Kobayashi R, Wakui H, Azushima K, et al. An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model. Kidney Int. 2017;91(5):1115-1125.
Kobayashi, R., Wakui, H., Azushima, K., Uneda, K., Haku, S., Ohki, K., Haruhara, K., Kinguchi, S., Matsuda, M., Ohsawa, M., Toya, Y., Nishiyama, A., Yamashita, A., Tanabe, K., Maeshima, Y., Umemura, S., & Tamura, K. (2017). An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model. Kidney International, 91(5), 1115-1125. https://doi.org/10.1016/j.kint.2016.10.035
Kobayashi R, et al. An Angiotensin II Type 1 Receptor Binding Molecule Has a Critical Role in Hypertension in a Chronic Kidney Disease Model. Kidney Int. 2017;91(5):1115-1125. PubMed PMID: 28081856.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model. AU - Kobayashi,Ryu, AU - Wakui,Hiromichi, AU - Azushima,Kengo, AU - Uneda,Kazushi, AU - Haku,Sona, AU - Ohki,Kohji, AU - Haruhara,Kotaro, AU - Kinguchi,Sho, AU - Matsuda,Miyuki, AU - Ohsawa,Masato, AU - Toya,Yoshiyuki, AU - Nishiyama,Akira, AU - Yamashita,Akio, AU - Tanabe,Katsuyuki, AU - Maeshima,Yohei, AU - Umemura,Satoshi, AU - Tamura,Kouichi, Y1 - 2017/01/10/ PY - 2016/05/27/received PY - 2016/09/28/revised PY - 2016/10/27/accepted PY - 2017/1/14/pubmed PY - 2017/9/28/medline PY - 2017/1/14/entrez KW - chronic kidney disease KW - hypertension KW - renal tubules KW - renin–angiotensin system SP - 1115 EP - 1125 JF - Kidney international JO - Kidney Int. VL - 91 IS - 5 N2 - Angiotensin II type 1 receptor-associated protein (ATRAP) promotes AT1R internalization along with suppression of hyperactivation of tissue AT1R signaling. Here, we provide evidence that renal ATRAP plays a critical role in suppressing hypertension in a mouse remnant kidney model of chronic kidney disease. The effect of 5/6 nephrectomy on endogenous ATRAP expression was examined in the kidney of C57BL/6 and 129/Sv mice. While 129/Sv mice with a remnant kidney showed decreased renal ATRAP expression and developed hypertension, C57BL/6 mice exhibited increased renal ATRAP expression and resistance to progressive hypertension. Consequently, we hypothesized that downregulation of renal ATRAP expression is involved in pathogenesis of hypertension in the remnant kidney model of chronic kidney disease. Interestingly, 5/6 nephrectomy in ATRAP-knockout mice on the hypertension-resistant C57BL/6 background caused hypertension with increased plasma volume. Moreover, in knockout compared to wild-type C57BL/6 mice after 5/6 nephrectomy, renal expression of the epithelial sodium channel α-subunit and tumor necrosis factor-α was significantly enhanced, concomitant with increased plasma membrane angiotensin II type 1 receptor in the kidneys. Thus, renal ATRAP downregulation is involved in the onset and progression of blood pressure elevation caused by renal mass reduction, and implicates ATRAP as a therapeutic target for hypertension in chronic kidney disease. SN - 1523-1755 UR - https://www.unboundmedicine.com/medline/citation/28081856/An_angiotensin_II_type_1_receptor_binding_molecule_has_a_critical_role_in_hypertension_in_a_chronic_kidney_disease_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(16)30650-0 DB - PRIME DP - Unbound Medicine ER -