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(Hypertension. 2007;49:542.)
© 2007 American Heart Association, Inc.
Original Articles |
From the Department of Human Biology (G.H.G., J.W.E.J., E.E.B., W.H.M.S., M.A.v.B.), Nutrition and Toxicology Research Institute Maastricht, and the Department of Pharmacology and Toxicology (P.M.S.), Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands.
Correspondence to Gijs H. Goossens, Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, Universiteitssingel 50, 6229 ER Maastricht, PO Box 616, 6200 MD Maastricht, the Netherlands. E-mail G.Goossens{at}hb.unimaas.nl
The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of ß-adrenergic stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic ß-adrenergic stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during ß-adrenergic stimulation (12.6±1.5 versus 8.1±1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during ß-adrenergic stimulation (both P<0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during ß-adrenergic stimulation in obese subjects (both P<0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during ß-adrenergic stimulation, which may contribute to the increased plasma Ang II concentrations during ß-adrenergic stimulation in obese subjects.
Key Words: angiotensin ß-adrenergic receptors obesity renin sympathetic nervous system
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