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Articles in PresS, published online ahead of print November 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00625.2002
Submitted on July 22, 2002
Accepted on October 30, 2002
1 Department of Medicine, Northwestern University, Chicago, IL, USA
2 Department of Pathology, Northwestern University, Chicago, IL, USA
3 Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: a-sahai{at}northwestern.edu.
We examined the effect of hypoxia and high glucose (HG) on Ang II type I (AT1) receptor expression and proliferation in cultured vascular smooth muscle (VSM) cells. Quiescent cells exposed to hypoxia in a serum-free DME/F12 medium for 6-24 hours induced a progressive increase in AT1 mRNA expression. Cells exposed to 24 hours of hypoxia also resulted in a significant increase in Ang II receptor binding as assessed with 125I-labeled Ang II. Treatment with Ang II (1 µmol/l) for 24 hours under normoxic conditions caused ~ 1.5 fold increase in both DNA synthesis and cell number, which were enhanced to ~ 3.0 fold under hypoxic conditions. An AT1 receptor antagonist (losartan, 10 µmol/l) blocked the Ang II-induced increase in DNA synthesis under both normoxic and hypoxic conditions. Incubations in HG medium (25 mmol/l) for 12-24 hours under normoxic conditions induced ~ 2.5 fold increase in AT1 mRNA levels, which was markedly enhanced by hypoxia to ~ 5.5 fold at 12 hours and ~ 8.5 fold at 24 hours, respectively. Ang II under HG-normoxic conditions caused a complete down-regulation of AT1 expression, which was prevented by hypoxia. These results demonstrate an upregulation of AT1 receptor expression by hypoxia and HG in cultured VSM cells, and suggest a mechanism for enhanced Ang II-induced VSM cell proliferation and to the development of atherosclerosis in diabetes.
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