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Intranephron Distribution and Regulation of Endothelin-Converting Enzyme-1 in Cyclosporin A-Induced Acute Renal Failure in Rats

YUSHI NAKAYAMA^*, HIROSHI NONOGUCHI^*, SHIGERU KIYAMA^*, MIKA IKEBE^*, YUKA TASHIMA^*, KOHEI SHIMADA, KAZUHIKO TANZAWA and KIMIO TOMITA^*

^* Third Department of Internal Medicine, Kumamoto University School of Medicine, Kumamoto, Japan
Biological Research Laboratories, Sankyo Co., Tokyo, Japan.

Correspondence to Dr. Yushi Nakayama, Third Department of Internal Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto, Kumamoto 860-8556, Japan. Phone: 81 96 373 5164; Fax: 81 96 366 8458; E-mail: nono{at}kaiju.medic.kumamoto-u.ac.jp

Abstract. Endothelin-1 (ET-1) is thought to play a significant role in acute renal failure induced by cyclosporin A (CsA). The cDNA sequence encoding endothelin-converting enzyme-1 (ECE-1), which produces the active form of ET-1 from big ET-1, was recently reported. To elicit the role of ECE-1 in the glomerular and tubular dysfunction induced by CsA, the effects of CsA on mRNA and protein expression of ECE-1 in rat kidney and on mRNA expression of prepro-ET-1 and ET A- and B-type receptors in glomeruli were studied. ECE-1 mRNA was detected in glomeruli and in whole nephron segments. ECE-1 mRNA expression was downregulated in all nephron segments at 24 h after CsA injection. Protein levels were also downregulated in glomeruli and in the outer and inner medulla. CsA rapidly increased prepro-ET-1 mRNA expression in glomeruli at 30 to 60 min after injection; this rapid increase was followed by an increase in plasma ET-1 levels. These increases were followed by decreased expression of ECE-1, ET A-type receptor, and ET B-type receptor mRNA at 6 h after injection, and serum creatinine levels were increased at 24 h after CsA injection. It is suggested that downregulation of glomerular and tubular ECE-1 expression may be caused by increased ET-1 synthesis in CsA-induced acute renal failure.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673