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1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA
* To whom correspondence should be addressed. E-mail: jnaik{at}physiology.umsmed.edu.
Obesity, insulin resistance, dyslipidemia, and hypertension are components of the pathophysiological state known as metabolic syndrome. Adrenergic vasoconstriction is mediated though increases in cytosolic Ca2+ and the myofilaments sensitivity to Ca2+. In pathophysiological states, there is an enhanced role for ROK-mediated increases in Ca2+-sensitivity of the contractile apparatus. Thus, we hypothesized that there is a greater role for Rho kinase (ROK)-mediated increases in Ca2+-sensitivity in 
1-adrenergic vasoconstriction in arteries from obese Zucker (OZ) rats. Therefore, small gracilis muscle arteries from 11-12 wk and 16-18 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+] were measured in response to phenylephrine (PE), the thromboxane mimetic U-46619, and KCl. 1-adrenergic vasoconstriction was similar between 11-12 wk old lean and obese animals, and greater in older obese animals compared to control. PE induced increases in VSM cell [Ca2+] were blunted in OZ animals compared to lean controls in both age groups of animals. KCl and U-46619 elicited similar vasoconstriction and VSM cell [Ca2+] in both groups. ROK inhibition attenuated PE vasoconstriction to a greater degree in arteries from 11-12 wk old OZ rats compared to lean animals, ROK inhibition in arteries from older rats right-shifted both concentration response curves to the same point. Total RhoA and ROK protein expression was similar between groups. These results suggest an enhanced role for the ROK pathway in 1-adrenergic vasoconstriction in metabolic syndrome.
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