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Articles in PresS, published online ahead of print October 22, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00080.2001
Submitted on March 8, 2001
Accepted on October 16, 2001
1 College of Veterinary Medicine, Chonnam National University, Kwangju, Korea, Republic of
* To whom correspondence should be addressed. E-mail: hjhan{at}chonnam.chonnam.ac.kr.
Renin-angiotensin system plays an important role in the development of diabetic nephropathy. Although the expression of renin and angiotensin-converting enzyme in diabetes mellitus has been well characterized, no information is available regarding angiotensin receptor regulation. Thus, we investigated signal pathways involved in high glucose-induced downregulation of ANG II binding in the primary cultured renal proximal tubule cells. Twenty five mM glucose, but not mannitol and L-glucose, induced downregulation of AT1 receptor due to a significant decline in Bmax with no significant change in Kd. Twenty five milimolar glucose also decreased AT1R mRNA adn protein levels. Twenty five mM glucose-induced increase of lipid peroxides formation was prevented by antioxidants, PKC inhibitors, or L type calcium channel blockers. These agents also blocked 25 mM glucose-induced downregulation of 125I-ANG II binding. In addition, 25 mM glucose increased transforming growth factor (TGF)-ß1 secretion and anti-TGF-ß antibody significantly blocked 25 mM glucose-induced downregulation of 125I-ANG II binding. Furthermore, 25 mM glucose-induced increase of TGF-ß1 secretion was inhibited by PKC inhibitors, L type calcium channel blocker, or antioxidants. In conclusion, high glucose may induce downregulation of 125I-ANG II binding via PKC-oxidative stress-TGF-ß1 signal cascade in primary cultured rabbit renal proximal tubule cells.
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