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(Hypertension. 1999;34:568-573.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the University "La Sapienza," Cattedra di I Clinica Medica, Andrea Cesalpino Foundation (C.F., G.D., M.P., G.D.M.), Rome; and the University of L'Aquila, Departments of Experimental (C.B.) and Internal (M.V., A.S.) Medicine, L'Aquila, Italy.
Correspondence to Claudio Ferri, MD, University "La Sapienza," Fondazione Andrea Cesalpino, Cattedra di I Clinica Medica, Servizio Divisionale di Fisiopatologia dell'Ipertensione Arteriosa, 00161 Roma, Italy. E-mail clferri{at}axrma.uniroma1.it
AbstractUpregulation of endothelial adhesion molecules is the earliest step of atherogenesis. Whether obesity induces endothelial adhesin upregulation is unknown. To address this topic, circulating vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor (vWF) concentrations were evaluated in 22 obese hypertensive (51.4±4.6 years [mean±SD age]), 19 obese normotensive (50.6±3.8 years), 18 nonobese hypertensive (52.3±3.9 years), and 16 nonobese normotensive (52.4±3.5 years) men without other risk factors or overt atherosclerosis. All measurements were repeated in the obese subgroups after weight loss induced by 12 weeks of caloric restriction. Basal circulating VCAM-1 levels were similar between the 2 obese groups but were higher (P<0.0001) than in the 2 nonobese groups. No differences were found between nonobese hypertensives and normotensives. Serum low density lipoprotein cholesterol was weakly correlated with plasma soluble VCAM-1 levels in pooled, obese subjects (r=0.362, P=0.02). Plasma soluble adhesin and vWF concentrations decreased significantly after weight loss in obese hypertensives (VCAM-1 P=0.03, ICAM-1 P=0.004, E-selectin P<0.0001, and vWF P=0.003) and normotensives (VCAM-1 P=0.04, ICAM-1 P=0.003, E-selectin P<0.0001, and vWF P<0.0001). Body mass index was correlated with plasma E-selectin concentrations at baseline and after weight loss in obese hypertensives (r=0.501, P=0.018 and r=0.466, P=0.03, respectively) and obese normotensives (r=0.523, P=0.021 and r=0.460, P=0.05, respectively). In conclusion, our data show that obesity per se induces early endothelial activation in hypertensive and normotensive men. Weight loss counteracted endothelial activation in both obese hypertensive and normotensive men.
Key Words: hypertension obesity endothelium adhesion molecules risk factors
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