Open AccessInvolvement of asymmetric dimethylarginine (ADMA) in tubulointerstitial ischaemia in the early phase of diabetic nephropathy
Author(s) -
Ryo Shibata,
Shinichiro Ueda,
Shoichi Yamagishi,
Y. Kaida,
Y. Matsumoto,
K. Fukami,
A. Hayashida,
H Matsuoka,
Seiya Kato,
Masumi Kimoto,
Seiya Okuda
Publication year - 2008
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfn630
Subject(s) - asymmetric dimethylarginine , medicine , diabetic nephropathy , endocrinology , nitric oxide , kidney , renal function , streptozotocin , nitric oxide synthase , nephropathy , diabetes mellitus , arginine , chemistry , biochemistry , amino acid
Decreased peritubular capillary (PTC) flow due to impaired endothelial function elicits tubulointerstitial ischaemia, thereby enhancing renal damage in chronic kidney disease, including diabetic nephropathy. Since nitric oxide (NO) is a vasodilator and known to play an important role in the maintenance of PTC flow, it is conceivable that asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, may cause tubulointerstitial ischaemia, thus being involved in the progression of diabetic nephropathy. In this study, we investigated whether overexpression of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme that degrades ADMA, could improve tubulointerstitial ischaemia in streptozotocin (STZ)-induced diabetic rats.
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