ASSA14-03-09 Impaired Dopamine D1Receptor-mediated Vasorelaxantion of Mesenteric Arteries in Obese Zucker Rats

Heart ◽  
2014 ◽  
Vol 101 (Suppl 1) ◽  
pp. A12.1-A12
Author(s):  
JJ Fu ◽  
Y Han ◽  
Z Wang ◽  
XJ Cheng ◽  
L Zhou ◽  
...  
Keyword(s):  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Obese Zucker Rats

Decreased epoxygenase and increased epoxide hydrolase expression in the mesenteric artery of obese Zucker rats

2005 ◽  
Vol 288 (1) ◽  
pp. R188-R196 ◽  
Author(s):  
Xueying Zhao ◽  
Aparajita Dey ◽  
Olga P. Romanko ◽  
David W. Stepp ◽  
Mong-Heng Wang ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Epoxyeicosatrienoic Acids ◽  
Obese Zucker Rat ◽  
Protein Expressions ◽  
Obese Zucker Rats ◽  
Cytochrome P 450

Previous studies suggest that epoxyeicosatrienoic acids (EETs) are vasodilators of the mesenteric artery; however, the production and regulation of EETs in the mesenteric artery remain unclear. The present study was designed 1) to determine which epoxygenase isoform may contribute to formation of EETs in mesenteric arteries and 2) to determine the regulation of mesenteric artery cytochrome P-450 (CYP) enzymes in obese Zucker rats. Microvessels were incubated with arachidonic acid, and CYP enzyme activity was determined. Mesenteric arteries demonstrate detectable epoxygenase and hydroxylase activities. Next, protein and mRNA expressions were determined in microvessels. Although renal microvessels express CYP2C23 mRNA and protein, mesenteric arteries lacked CYP2C23 expression. CYP2C11 and CYP2J mRNA and protein were expressed in mesenteric arteries and renal microvessels. In addition, mesenteric artery protein expression was evaluated in lean and obese Zucker rats. Compared with lean Zucker rats, mesenteric arterial CYP2C11 and CYP2J proteins were decreased by 38 and 43%, respectively, in obese Zucker rats. In contrast, soluble epoxide hydrolase mRNA and protein expressions were significantly increased in obese Zucker rat mesenteric arteries. In addition, nitric oxide-independent dilation evoked by acetylcholine was significantly attenuated in mesenteric arteries of obese Zucker rats. These data suggest that the main epoxygenase isoforms expressed in mesenteric arteries are different from those expressed in renal microvessels and that decreased epoxygenases and increased soluble epoxide hydrolase are associated with impaired mesenteric artery dilator function in obese Zucker rats.

scholarly journals Reduced Endothelium-Dependent Relaxation to Anandamide in Mesenteric Arteries from Young Obese Zucker Rats

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e63449 ◽  
Author(s):  
Nubia S. Lobato ◽  
Fernando P. Filgueira ◽  
Roshini Prakash ◽  
Fernanda R. Giachini ◽  
Adviye Ergul ◽  
...  
Keyword(s):  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Endothelium Dependent Relaxation

scholarly journals Oral supplementation of propionyl-l-carnitine reduces body weight and hyperinsulinaemia in obese Zucker rats

2009 ◽  
Vol 102 (8) ◽  
pp. 1145-1153 ◽  
Author(s):  
Carmen Mingorance ◽  
Maria Gonzalez del Pozo ◽  
Maria Dolores Herrera ◽  
Maria Alvarez de Sotomayor
Keyword(s):  
Insulin Resistance ◽  
Animal Model ◽  
Body Weight ◽  
Food Intake ◽  
Vascular Function ◽  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Acid Oxidation ◽  
Oral Glucose ◽  
Obese Zucker Rats

Propionyl-l-carnitine (PLC) is an SCFA esterified to carnitine that plays an important role in fatty acid oxidation and energy expenditure, in addition to having a protective effect on the endothelium. In order to evaluate the effect of PLC on an animal model of obesity, insulin resistance and, consequently, endothelial dysfunction, lean and obese Zucker rats (OZR) received either vehicle- or PLC-supplemented drinking water (200 mg/kg per d) for 20 weeks. Body weight, food intake, systolic blood pressure and heart rate were controlled weekly and an oral glucose tolerance test was performed. Fasting glucose, TAG, cholesterol, HDL, NEFA, adiponectin and insulin were analysed in serum. Visceral adipose tissue and liver were weighed and liver TAG liver composition was evaluated. Endothelial and vascular functions were assessed in the aorta and small mesenteric arteries by response to acetylcholine, sodium nitroprusside and phenylephrine (Phe); NO participation was evaluated after incubation with the NO synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME) and endothelial NOS protein expression by Western blotting. PLC decreased body-weight gain, food intake, adiposity, insulin serum concentration and TAG liver content and improved insulin resistance. Aortae from OZR receiving either vehicle or PLC exhibited a lower contractile response to Phe. PLC-treated OZR showed an enhanced release of endothelial NO upon the adrenergic stimulation. The protection of vascular function found after treatment with PLC in an animal model of insulin resistance supports the necessity of clinical trials showing the effect of l-carnitine supplements on metabolic disorders.

scholarly journals Impaired dopamine D1 receptor-mediated vasorelaxation of mesenteric arteries in obese Zucker rats

2014 ◽  
Vol 13 (1) ◽  
pp. 50 ◽  
Author(s):  
Jinjuan Fu ◽  
Yu Han ◽  
Hongyong Wang ◽  
Zhen Wang ◽  
Yukai Liu ◽  
...  
Keyword(s):  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Obese Zucker Rats

Targeting the Endothelial Ca2+ Toolkit to Rescue Endothelial Dysfunction in Obesity Associated-Hypertension

2020 ◽  
Vol 27 (2) ◽  
pp. 240-257 ◽  
Author(s):  
Francesco Moccia ◽  
Sharon Negri ◽  
Pawan Faris ◽  
Roberto Berra-Romani
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Endothelial Damage ◽  
Vascular Damage ◽  
Zucker Rats ◽  
Bibliographic Databases ◽  
Resistance Arteries ◽  
Small Resistance ◽  
Obese Zucker Rats ◽  
Transient Receptor

Background: Obesity is a major cardiovascular risk factor which dramatically impairs endothelium- dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g., acetylcholine, mainly depends on the reduced Nitric Oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect Endothelium-Dependent Hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca2+ signals drive NO release and trigger EDH. Methods: A structured search of bibliographic databases was carried out to retrieve the most influential, recent articles on the impairment of vasorelaxation in animal models of obesity, including obese Zucker rats, and on the remodeling of the endothelial Ca2+ toolkit under conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue Ca2+-dependent vasodilation. Results: We found evidence that the endothelial Ca2+ could be severely affected by obese vessels. This rearrangement could contribute to endothelial damage and is likely to be involved in the disruption of vasorelaxant mechanisms. However, several Ca2+-permeable channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be stimulated by several food components to stimulate vasorelaxation in obese individuals. Conclusion: The endothelial Ca2+ toolkit could be targeted to reduce vascular damage and rescue endothelium- dependent vasodilation in obese vessels. This hypothesis remains, however, to be probed on truly obese endothelial cells.

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