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1 Cardiovascular Research Center, University of Kentucky, Lexington, Kentucky, United States
2 Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States
3 Cardiovascular Research Center, University of Kentucky, Lexington, Kentucky, United States; University of Kentucky, Lexington, Kentucky, United States
4 Lexington, Kentucky, United States; Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States
* To whom correspondence should be addressed. E-mail: lcassis{at}uky.edu.
Adipose tissue has been recognized as an important source of angiotensinogen (AGT), in addition to the well defined contribution of the liver. The purpose of this study was to define the angiotensin II (AngII) receptors involved in the regulation of adipose AGT, and the relationship of this control to systemic AGT and/or angiotensin peptide concentrations. In LDL receptor deficient (LDLR-/-) male mice, adipose mRNA abundance of AGT was 68% of that in liver, the AT1a receptor (AT1aR) was 38% of liver, while mRNA abundance of AT2 receptor (AT2R) was 57% greater in adipose tissue. AGT and angiotensin peptide concentrations were decreased in plasma of AT1aR -/- mice and were paralleled by reductions in AGT expression in liver. In contrast, adipose AGT mRNA abundance was unaltered in AT1aR -/- mice. AT2R -/- mice exhibited elevated plasma angiotensin peptide concentrations and marked elevations in adipose AGT and AT1aR mRNA abundance. Increases in adipose AGT mRNA abundance in AT2R -/- mice were abolished by losartan. In contrast, liver AGT and AT1aR mRNA abundance were unaltered in AT2R -/- mice. Infusion of AngII for 28 days to LDLR -/- mice markedly increased adipose AGT and AT1aR mRNA, but did not alter their expression in liver. These results demonstrate that differential mRNA abundance of AT1a/AT2 receptors in adipose versus liver contributes to tissue-specific AngII-mediated regulation of AGT. Chronic infusion of AngII robustly stimulated AT1aR and AGT mRNA abundance in adipose tissue, suggesting that adipose tissue serves as a primary contributor to the activated systemic RAS.
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