Retraction：Effects of Pre- and Post-ischemic Treatments with FK409, a Nitric Oxide Donor, on Ischemia/Reperfusion-Induced Renal Injury and Endothelin-1 Production in Rats
| Autor: | Hayato Kurata, Junji Takayama, Masanori Takaoka, Mamoru Ohkita, Yasuo Matsumura, Atsushi Nakajima, Kyoko Ueda |
|---|---|
| Rok vydání: | 2006 |
| Předmět: | |
| Zdroj: | Biological and Pharmaceutical Bulletin. 29:577-579 |
| ISSN: | 1347-5215 0918-6158 |
| DOI: | 10.1248/bpb.29.577 |
| Popis: | We have demonstrated that ischemic acute renal failure (ARF) is attenuated by pre-ischemic treatment with a spontaneous nitric oxide (NO) donor, (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409). In the present study, we evaluated the effect of post-ischemic treatment with FK409 on ARF, compared with the pre-ischemic treatment effect. Ischemic ARF was induced by occlusion of the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. At 24 h after reperfusion, renal function in untreated ARF rats markedly decreased. In addition, increases in renal contents of endothelin-1 (ET-1), a deleterious mediator in the pathogenesis of ischemic ARF, were evident in untreated ARF rats at 24 h after reperfusion. Pre-ischemic treatment with FK409 (1 or 3 mg/kg, i.v.) at 5 min before ischemia attenuated ischemia/reperfusion-induced renal dysfunction and increased ET-1 contents after reperfusion. In contrast, post-ischemic treatment with FK409 (3 or 10 mg/kg, i.v.) at 6 h after reperfusion aggravated the renal injury, but did not affect the increased ET-1 content after reperfusion. These results suggest that pre-ischemic treatment with FK409 exerts renoprotective effects on ischemic ARF, probably through the suppression of renal ET-1 overproduction, whereas post-ischemic treatment with the NO donor worsens the ischemia/reperfusion-induced renal injury, through mechanisms unrelated to the ET-1 production after reperfusion. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|