| First Author | Matsumura Y | Year | 2002 |
| Journal | Clin Sci (Lond) | Volume | 103 Suppl 48 |
| Pages | 389S-392S | PubMed ID | 12193129 |
| Mgi Jnum | J:105954 | Mgi Id | MGI:3617063 |
| Doi | 10.1042/CS103S389S | Citation | Matsumura Y, et al. (2002) Pathophysiological roles of Ca(2+) overload via the Na(+)/Ca(2+) exchanger and endothelin-1 overproduction in ischaemia/reperfusion-induced acute renal failure. Clin Sci (Lond) 103 Suppl 48:389S-392S |
| abstractText | Using Na(+)/Ca(2+) exchanger (NCX1)-deficient mice, the pathophysiological role of Ca(2+) overload via the reverse mode of the Na(+)/Ca(2+) exchanger in ischaemia/reperfusion-induced renal injury was investigated. Since NCX1(-/-) homozygous mice die of heart failure before birth, we utilized NCX1(+/-) heterozygous mice. The ischaemia/reperfusion-induced renal dysfunction in heterozygous mice were significantly attenuated compared with cases in wild-type mice. Also, histological renal damage such as tubular necrosis and proteinaceous casts in tubuli in heterozygous mice were much less than that in wild-type mice. Ca(2+) deposition in necrotic tubular epithelium was observed more markedly in wild-type than in heterozygous mice. The increase in renal endothelin-1 (ET-1) content was significantly greater in wild-type than in heterozygous mice, and this reflected the difference in immunohistochemical ET-1 localization in necrotic tubular epithelium. We conclude that Ca(2+) overload via the reverse-mode of Na(+)/Ca(2+) exchange, followed by renal ET-1 overproduction, plays an important role in the pathogenesis of ischaemia/reperfusion-induced acute renal failure. |
