Jennifer Dearman

Publications (2)6.28 Total impact

• Article: K(ATP)-mediated Vasodilation is Impaired in Obese Zucker Rats.

  Benjamin Hodnett, Lusha Xiang, Jennifer Dearman, Cory Carter, Robert Hester
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  ABSTRACT: Objective: Skeletal muscle blood flow during exercise is impaired in obesity. We tested the hypothesis that the attenuated vasodilation in skeletal muscle arterioles of obese Zucker rats (OZR) is due to altered K(ATP) channel-mediated vasodilation. Materials and Methods: K(ATP) channel function was determined in isolated skeletal muscle arterioles in response to the K(ATP) opener cromakalim (0.1-10 mu M) during normal myogenic tone and alpha -adrenergic-mediated tone (0.1 mu M phenylephrine). The spinotrapezius muscle was prepared and the vasodilatory responses to muscle stimulation or iloprost (0.028-2.8 mu M) were observed before and after the application of the K(ATP) inhibitor, glibenclamide (10 mu M). Channel subunit expression was determined by using western blot analyses. Results: Cromakalim concentration-response curves were shifted in OZR as compared to lean controls. OZR exhibited impaired functional and iloprost-induced vasodilation as compared to the lean controls. Glibenclamide inhibited the functional and iloprost-induced dilation in the lean rats with no effects in the obese animals. Channel subunit expression was similar in femoral arteries. Conclusion:The impaired functional vasodilation in the OZR is associated with altered K(ATP) channel sensitivity.
  Microcirculation 07/2008; · 2.57 Impact Factor
• Article: Insulin resistance and impaired functional vasodilation in obese Zucker rats.

  Lusha Xiang, Jennifer Dearman, Sean R Abram, Cory Carter, Robert L Hester
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  ABSTRACT: Individuals with metabolic syndrome exhibit insulin resistance and an attenuated functional vasodilatory response to exercise. We have shown that impaired functional vasodilation in obese Zucker rats (OZRs) is associated with enhanced thromboxane receptor (TP)-mediated vasoconstriction. We hypothesized that insulin resistance, hyperglycemia/hyperlipidemia, and the resultant ROS are responsible for the increased TP-mediated vasoconstriction in OZRs, resulting in impaired functional vasodilation. Eleven-week-old male lean Zucker rats (LZRs) and OZRs were fed normal rat chow or chow containing rosiglitazone (5 mg.kg(-1).day(-1)) for 2 wk. In another set of experiment, LZRs and OZRs were treated with 2 mM tempol (drinking water) for 7-10 days. After the treatments, spinotrapezius muscles were prepared, and arcade arteriolar diameters were measured following muscle stimulation and arachidonic acid (AA) application (10 muM) in the absence and presence of the TP antagonist SQ-29548 (1 muM). OZRs exhibited higher insulin, glucose, triglyceride, and superoxide levels and increased NADPH oxidase activity compared with LZRs. Functional and AA-induced vasodilations were impaired in OZRs. Rosiglitazone treatment improved insulin, glucose, triglyceride, and superoxide levels as well as NADHP oxidase activity in OZRs. Both rosiglitazone and tempol treatment improved vasodilatory responses in OZRs with no effect in LZRs. SQ-29548 treatment improved vasodilatory responses in nontreated OZRs with no effect in LZRs or treated OZRs. These results suggest that insulin resistance and the resultant increased ROS impair functional dilation in OZRs by increasing TP-mediated vasoconstriction.
  AJP Heart and Circulatory Physiology 05/2008; 294(4):H1658-66. · 3.71 Impact Factor