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1 Division of Pharmaceutical Sciences, University of Kentucky, Lexington, KY, USA
2 Department of Internal Medicine, University of Kentucky, Lexington, KY, USA; Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY, USA
3 Graduate Center for Biomedical Engineering, University of Kentucky, Lexington, KY, USA
4 Department of Physiology, University of Kentucky, Lexington, KY, USA
5 Division of Pharmaceutical Sciences, University of Kentucky, Lexington, KY, USA; Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: lcassis{at}uky.edu.
In obesity-related hypertension, activation of the renin-angiotensin system (RAS) has been reported despite marked fluid volume expansion. Adipose tissue expresses components of the RAS, and is markedly expanded in obesity. This study evaluated changes in components of the adipose and systemic RAS in diet-induced obese, hypertensive rats. The RAS was quantified in adipose tissue, and compared to primary sources for the circulating RAS. Male, Sprague Dawley rats were fed either a low fat (LF, 11% Kcal as fat) or moderately high fat (MHF, 32% kcal as fat) diet for 11 weeks. After 8 weeks, rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups based on their body weight gain (Body weight; OR: 566 ± 10, OP: 702 ± 20 g; P<0.05). Mean arterial blood pressure (MAP) was increased in OP rats (LF: 97 ± 2, OR: 97 ± 2, OP: 105 ± 1 mmHg; P<0.05). Quantification of mRNA expression by real-time PCR demonstrated a selective increase (2-fold) in angiotensinogen gene expression in retroperitoneal adipose tissue from OP rats versus OR and LF. Similarly, plasma angiotensinogen concentration was increased in OP rats (LF: 390 ± 48, OR: 355 ± 24, OP: 530 ± 22 ng/ml; P<0.05). In contrast, other components of the RAS were not altered in OP rats. Marked increases in the plasma concentrations of angiotensin peptides were observed in OP rats (AngII; LF: 95 ± 31, OR: 59 ± 20, OP: 295 ± 118 pg/ml; P<0.05). These results demonstrate increased activity of the adipose and systemic RAS in obesity-related hypertension.
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