Involvement of Nitric Oxide in the Suppressive Effect of 17??-Estradiol on Endothelin-1 Overproduction in Ischemic Acute Renal Failure
| Autor: | Yujiro Shibata, Yasuo Matsumura, Daisuke Maekawa, Chika Kuwahara, Masanori Takaoka |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_specialty Microdialysis Time Factors medicine.medical_treatment Ischemia Kidney Kidney Function Tests Nitric Oxide urologic and male genital diseases Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound In vivo Internal medicine medicine Animals Enzyme Inhibitors Pharmacology Endothelin-1 Estradiol biology business.industry Acute Kidney Injury medicine.disease Endothelin 1 Nephrectomy Rats Nitric oxide synthase Disease Models Animal NG-Nitroarginine Methyl Ester Endocrinology medicine.anatomical_structure chemistry Reperfusion Injury Anesthesia biology.protein Nitric Oxide Synthase Cardiology and Cardiovascular Medicine business |
| Zdroj: | Journal of Cardiovascular Pharmacology. 44:S459-S461 |
| ISSN: | 0160-2446 |
| Popis: | It is known that 17beta-estradiol (E2-beta) increases the production of nitric oxide. We have demonstrated that E2-beta prevents renal injury and suppresses renal endothelin-1 overproduction in ischemic acute renal failure in rats. In the present study, we investigated whether N(G)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, can reverse the effect of E2-beta in ischemic acute renal failure. Ischemic acute renal failure was induced by clamping the left renal artery and vein for 45 minutes followed by reperfusion, 2 weeks after contralateral nephrectomy. Pre-ischemic treatment with E2-beta (100 microg/kg, intravenously) attenuated the ischemia/ reperfusion-induced renal dysfunction and suppressed the increment of renal endothelin-1 content 24 hours after reperfusion. The effects of E2-beta on renal dysfunction and increased endothelin-1 content in acute renal failure rats were reversed by pretreatment with N(G)-nitro-L-arginine methyl ester (0.3 mg/kg, intravenously). An in vivo microdialysis study revealed that the concentration of nitric oxide metabolites in the kidney was reduced during ischemia, and quickly recovered after reperfusion in E2-beta-treated acute renal failure rats, compared with cases in untreated acute renal failure rats. This recovery of renal nitric oxide metabolite concentration with E2-beta was abolished by the pretreatment with N(G)-nitro-Larginine methyl ester. These findings suggest that nitric oxide is closely related to suppressive effect of E2-beta on renal endothelin-1 overproduction in acute renal failure rats and this suppression is probably involved in the beneficial effect of E2-beta on ischemia/reperfusion-induced renal injury. |
| Databáze: | OpenAIRE |
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