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Metabolic Syndrome

Enhanced role for RhoA-associated kinase in adrenergic-mediated vasoconstriction in gracilis arteries from obese Zucker rats

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi

Submitted 8 April 2005 ; accepted in final form 29 August 2005

Obesity, insulin resistance, dyslipidemia, and hypertension are components of the pathophysiological state known as metabolic syndrome. Adrenergic vasoconstriction is mediated through increases in cytosolic Ca²⁺ and the myofilaments' sensitivity to Ca²⁺. In many pathophysiological states, there is an enhanced role for Rho kinase (ROK)-mediated increases in Ca²⁺ sensitivity of the contractile apparatus. Thus we hypothesized that there is a greater role for ROK-mediated increases in Ca²⁺ sensitivity in ₁-adrenergic vasoconstriction in arteries from obese Zucker (OZ) rats. Therefore, small gracilis muscle arteries from 11- to 12-wk-old and 16- to 18-wk-old lean and OZ rats were isolated, cannulated, and pressurized to 75 mmHg. For some experiments, vessels were loaded with fura 2-AM. Changes in luminal diameter and vessel wall Ca²⁺ concentration ([Ca²⁺]) were measured in response to phenylephrine (PE), the thromboxane mimetic U-46619, and KCl. ₁-Adrenergic vasoconstriction was similar between 11- to 12-wk-old lean and obese animals and greater in older obese animals compared with controls. PE-induced increases in vascular smooth muscle cell [Ca²⁺] were blunted in OZ animals compared with lean controls in both age groups of animals. KCl and U-46619 elicited similar vasoconstriction and vascular smooth muscle cell [Ca²⁺] in both groups. ROK inhibition attenuated PE vasoconstriction to a greater degree in arteries from 11- to 12-wk-old OZ rats compared with lean animals; ROK inhibition in arteries from older rats right shifted both concentration-response curves to the same point. Total RhoA and ROK protein expressions were similar between groups. These results suggest an enhanced role for the ROK pathway in ₁-adrenergic vasoconstriction in metabolic syndrome.

vascular smooth muscle; vascular reactivity; isolated vessel; fura 2; phenylephrine; Type 2 diabetes

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