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1 Division of Pharmaceutical Sciences, University of Kentucky, Lexington, KY, USA
2 Graduate Center for Biomedical Engineering, University of Kentucky, Lexington, KY, USA
3 Department of Physiology, University of Kentucky, Lexington, KY, USA
4 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.
Previous studies in our laboratory demonstrated that rats exhibiting obesity in response to a moderately high fat (MHF) diet developed hypertension associated with activation of the local and systemic renin-angiotensin system (RAS). In this study we examined the effect of the angiotensin type 1 (AT1) receptor antagonist, losartan, on blood pressure in obesity-prone (OP) and obesity-resistant (OR) rats fed a MHF diet. Using telemetry monitoring, we characterized the evolution of blood pressure elevations during the development of obesity. Male Sprague-Dawley rats were implanted with telemetry transducers for chronic monitoring of blood pressure and baseline measurements were obtained. Rats were then switched to the MHF diet (32% kcal as fat) and were segregated into OP and OR groups at week 5. At week 9 on the MHF diet, OP rats exhibited significantly greater 24 hour mean arterial blood pressure (MAP) compared to OR (OP: 105 ± 4, OR: 96 ± 2 mm Hg, P<0.05). Elevations in blood pressure in OP rats were manifest as an increase in systolic pressure. Administration of losartan to all rats at week 9 resulted in a reduction in blood pressure; however, losartan had the greatest effect in OP rats (percent decrease in MAP by losartan; OP: 19 ± 4, OR: 10 ± 2 %, P<0.05). These results demonstrate that elevations in blood pressure occur subsequent to established obesity in rats fed a high fat diet. Moreover, these results demonstrate the ability of losartan to reverse the blood pressure increase from diet-induced obesity, supporting a primary role for the RAS in obesity-associated hypertension.
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