| First Author | Hisamichi M | Year | 2017 |
| Journal | FASEB J | Volume | 31 |
| Issue | 1 | Pages | 72-84 |
| PubMed ID | 27663860 | Mgi Jnum | J:267584 |
| Mgi Id | MGI:6267720 | Doi | 10.1096/fj.201600684RR |
| Citation | Hisamichi M, et al. (2017) Role of angiotensin II type 1a receptor in renal injury induced by deoxycorticosterone acetate-salt hypertension. FASEB J 31(1):72-84 |
| abstractText | The aim of this study was to investigate the in vivo role of angiotensin II type 1a (AT1a) receptor in renal damage as a result of hypertension by using transgenic mice with AT1a receptor gene disruption. Transgenic mice that express human liver-type fatty acid binding protein (L-FABP) with or without disruption of the AT1a receptor gene (L-FABP(+/-) AT1a(-/-), and L-FABP(+/-) AT1a(+/+), respectively) were used with urinary L-FABP as an indicator of tubulointerstitial damage. Those female mice were administered subcutaneously deoxycorticosterone acetate (DOCA)-salt tablets plus drinking water that contained 1% saline for 28 d after uninephrectomy. In L-FABP(+/-) AT1a(+/+) mice that received DOCA-salt treatment, hypertension was induced and slight expansion of glomerular area, glomerular sclerosis, and tubulointerstitial damage were observed. In L-FABP(+/-) AT1a(-/-) mice that received DOCA-salt treatment, hypertension was similarly induced and the degree of glomerular damage was significantly more severe than in L-FABP(+/-) AT1a(+/+)-DOCA mice. Urinary L-FABP levels were significantly higher in L-FABP(+/-) AT1a(-/-)-DOCA mice compared with those in L-FABP(+/-) AT1a(+/+)-DOCA mice. Hydralazine treatment significantly attenuated renal damage that was found in L-FABP(+/-) AT1a(-/-)-DOCA mice along with a reduction in blood pressure. In summary, activation of the AT1a receptor may contribute to maintenance of the glomerular structure against hypertensive renal damage.-Hisamichi, M., Kamijo-Ikemori, A., Sugaya, T., Ichikawa, D., Natsuki, T., Hoshino, S., Kimura, K., Shibagaki, Y. Role of angiotensin II type 1a receptor in renal injury induced by deoxycorticosterone acetate-salt hypertension. |
