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Am J Physiol Renal Physiol (October 23, 2001). doi:10.1152/ajprenal.00080.2001
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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

Mechanism of angiotensin II binding downregulation by high glucose in primary renal proximal tubule cells

Park Soo Hyun1 and Han Ho Jae1*

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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