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Am J Physiol Regul Integr Comp Physiol 290: R601-R608, 2006. First published November 10, 2005; doi:10.1152/ajpregu.00308.2005
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Metabolic Syndrome

Metabolic syndrome increases endogenous carbon monoxide production to promote hypertension and endothelial dysfunction in obese Zucker rats

Fruzsina K. Johnson,1 Robert A. Johnson,1 William Durante,2 Keith E. Jackson,1 Blake K. Stevenson,1 and Kelly J. Peyton2

1Tulane Hypertension and Renal Center of Excellence, and Department of Physiology, Tulane University Health Sciences Center, New Orleans, Lousiana; 2Micheal E. DeBakey Veterans Affairs Medical Center, and Departments of Medicine and Pharmacology, Baylor College of Medicine, Houston, Texas

Submitted 2 May 2005 ; accepted in final form 8 November 2005

Vascular heme oxygenase (HO) metabolizes heme to form carbon monoxide (CO). Increased heme-derived CO inhibits nitric oxide synthase and can contribute to hypertension via endothelial dysfunction in Dahl salt-sensitive rats. Obese Zucker rats (ZR) are models of metabolic syndrome. This study tests the hypothesis that endogenous CO formation is increased and contributes to hypertension and endothelial dysfunction in obese ZR. Awake obese ZR showed increased respiratory CO excretion, which was lowered by HO inhibitor administration [zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) 25 µmol·kg–1·24 h–1 ip]. In awake obese ZR, chronically instrumented with femoral arterial catheters, blood pressure was elevated but was decreased by the HO inhibitor ZnDPBG. Body weight, blood glucose, glycated hemoglobin, plasma insulin, total and LDL cholesterol, oxidized LDL, and triglyceride levels were elevated in obese ZR, and, except for LDL cholesterol, were unchanged by HO inhibition. Total HO-1 protein levels were not different between lean and obese ZR aortas. In vitro experiments used isolated skeletal muscle arterioles with constant pressure and no flow, or constant midpoint, but altered endpoint pressures to establish graded levels of luminal flow. In obese ZR arterioles, responses to ACh and flow were attenuated. Acute in vitro pretreatment with an HO inhibitor, chromium mesoporphyrin, enhanced ACh and flow-induced dilation and abolished the differences between groups. Furthermore, exogenous CO prevented the restoration of flow-induced dilation by the HO inhibitor in obese ZR arterioles. These results suggest that HO-derived CO production is increased and promotes hypertension and arteriolar endothelial dysfunction in obese ZR with metabolic syndrome independent of affecting metabolic parameters.

heme oxygenase; blood pressure; arterioles; vascular tone regulation


Address for reprint requests and other correspondence: F. K. Johnson, Dept. of Physiology, Tulane Univ. Health Sciences Center, 1430 Tulane Ave., SL-39, New Orleans, LA 70112 (e-mail: fjohnson{at}cvlabs.org)




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