Nitric oxide synthase levels in obese Zucker rats

1996 ◽  
Vol 209 (2) ◽  
pp. 137-139 ◽  
Author(s):  
John E. Morley ◽  
Michael B. Mattammal
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Oxide Synthase

scholarly journals Increased vascular thromboxane generation impairs dilation of skeletal muscle arterioles of obese Zucker rats with reduced oxygen tension

2008 ◽  
Vol 295 (4) ◽  
pp. H1522-H1528 ◽  
Author(s):  
Adam G. Goodwill ◽  
Milinda E. James ◽  
Jefferson C. Frisbee
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Superoxide Dismutase ◽  
Arachidonic Acid ◽  
Polyethylene Glycol ◽  
Nitric Oxide Synthase ◽  
Oxidant Stress ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Oxide Synthase

This study determined if altered vascular prostacyclin (PGI2) and/or thromboxane A2 (TxA2) production with reduced Po2 contributes to impaired hypoxic dilation of skeletal muscle resistance arterioles of obese Zucker rats (OZRs) versus lean Zucker rats (LZRs). Mechanical responses were assessed in isolated gracilis muscle arterioles following reductions in Po2 under control conditions and following pharmacological interventions inhibiting arachidonic acid metabolism and nitric oxide synthase and alleviating elevated vascular oxidant stress. The production of arachidonic acid metabolites was assessed using pooled arteries from OZRs and LZRs in response to reduced Po2. Hypoxic dilation, endothelium-dependent in both strains, was attenuated in OZRs versus LZRs. Nitric oxide synthase inhibition had no significant impact on hypoxic dilation in either strain. Cyclooxygenase inhibition dramatically reduced hypoxic dilation in LZRs and abolished responses in OZRs. Treatment of arterioles from OZRs with polyethylene glycol-superoxide dismutase improved hypoxic dilation, and this improvement was entirely cyclooxygenase dependent. Vascular PGI2 production with reduced Po2 was similar between strains, although TxA2 production was increased in OZRs, a difference that was attenuated by treatment of vessels from OZRs with polyethylene glycol-superoxide dismutase. Both blockade of PGH2/TxA2 receptors and inhibition of thromboxane synthase increased hypoxic dilation in OZR arterioles. These results suggest that a contributing mechanism underlying impaired hypoxic dilation of skeletal muscle arterioles of OZRs may be an increased vascular production of TxA2, which competes against the vasodilator influences of PGI2. These results also suggest that the elevated vascular oxidant stress inherent in metabolic syndrome may contribute to the increased vascular TxA2 production and may blunt vascular sensitivity to PGI2.

Anorectic activity of NG-nitro-L-arginine, an inhibitor of brain nitric oxide synthase, in obese Zucker rats

1993 ◽  
Vol 230 (1) ◽  
pp. 125-128 ◽  
Author(s):  
Francesco Squadrito ◽  
Gioacchino Calapai ◽  
Domenico Cucinotta ◽  
Domenica Altavilla ◽  
Basilia Zingarelli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Oxide Synthase ◽  
Brain Nitric Oxide ◽  
Anorectic Activity

Sex Differences in Renal Nitric Oxide Synthase, NAD(P)H Oxidase, and Blood Pressure in Obese Zucker Rats

2007 ◽  
Vol 4 (3) ◽  
pp. 214-229 ◽  
Author(s):  
Shahla Riazi ◽  
Veerendra K. Madala-Halagappa ◽  
Ana Paula Dantas ◽  
Xinqun Hu ◽  
Carolyn A. Ecelbarger
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sex Differences ◽  
Nitric Oxide Synthase ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Oxide Synthase

scholarly journals Estrogen has opposing effects on vascular reactivity in obese, insulin-resistant male Zucker rats

2002 ◽  
Vol 92 (5) ◽  
pp. 2035-2044 ◽  
Author(s):  
Esther M. Brooks-Asplund ◽  
Artin A. Shoukas ◽  
Soon-Yul Kim ◽  
Sean A. Burke ◽  
Dan E. Berkowitz
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Expression ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Zucker Rats ◽  
Sham Operation ◽  
Insulin Resistant ◽  
Obese Rats ◽  
Oxide Synthase

We hypothesized that estradiol treatment would improve vascular dysfunction commonly associated with obesity, hyperlipidemia, and insulin resistance. A sham operation or 17β-estradiol pellet implantation was performed in male lean and obese Zucker rats. Maximal vasoconstriction (VC) to phenylephrine (PE) and potassium chloride was exaggerated in control obese rats compared with lean rats, but estradiol significantly attenuated VC in the obese rats. Estradiol reduced the PE EC50 in all groups. This effect was cyclooxygenase independent, because preincubation with indomethacin reduced VC response to PE similarly in a subset of control and estrogen-treated lean rats. Endothelium-independent vasodilation (VD) to sodium nitroprusside was similar among groups, but endothelium-dependent VD to ACh was significantly impaired in obese compared with lean rats. Estradiol improved VD in lean and obese rats by decreasing EC50 but impaired function by decreasing maximal VD. The shift in EC50 corresponded to an upregulation in nitric oxide synthase III protein expression in the aorta of the estrogen-treated obese rats. In summary, estrogen treatment improves vascular function in male insulin-resistant, obese rats, partially via an upregulation of nitric oxide synthase III protein expression. These effects are counteracted by adverse factors, such as hyperlipidemia and, potentially, a release of an endothelium-derived contractile agent.

Impaired dilation of skeletal muscle microvessels to reduced oxygen tension in diabetic obese Zucker rats

2001 ◽  
Vol 281 (4) ◽  
pp. H1568-H1574 ◽  
Author(s):  
Jefferson C. Frisbee
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Superoxide Anion ◽  
Zucker Rats ◽  
Radical Scavengers ◽  
Resistance Arteries ◽  
Nitric Oxide Release ◽  
Obese Zucker Rats ◽  
Arterial Dilation ◽  
Oxide Synthase

This study determined alterations to hypoxic dilation of isolated skeletal muscle resistance arteries (gracilis arteries; viewed via television microscopy) from obese Zucker rats (OZR) compared with lean Zucker rats (LZR). Hypoxic dilation was reduced in OZR compared with LZR. Endothelium removal and cyclooxygenase inhibition (indomethacin) severely reduced this response in both groups, although nitric oxide synthase inhibition ( N ω-nitro-l-arginine methyl ester) reduced dilation in LZR only. Treatment of vessels with a PGH2-thromboxane A2 receptor antagonist had no effect on hypoxic dilation in either group. Arterial dilation to arachidonic acid, iloprost, acetylcholine, and sodium nitroprusside was reduced in OZR versus LZR, although dilation to forskolin and aprikalim was unaltered. Treatment of arteries from OZR with oxidative radical scavengers increased dilation to hypoxia and agonists, with no effect on responses in LZR. The restored hypoxic dilation in OZR was abolished by indomethacin. These results suggest that hypoxic dilation of skeletal muscle microvessels from LZR represents the summated effects of prostanoid and nitric oxide release, whereas the impaired response of vessels in OZR may reflect scavenging of PGI2 by superoxide anion.

scholarly journals Wild blueberry consumption affects aortic vascular function in the obese Zucker rat

2014 ◽  
Vol 39 (2) ◽  
pp. 255-261 ◽  
Author(s):  
Stefano Vendrame ◽  
Aleksandra S. Kristo ◽  
Dale A. Schuschke ◽  
Dorothy Klimis-Zacas
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Biomechanical Properties ◽  
Diet Group ◽  
Zucker Rats ◽  
Zucker Rat ◽  
The Metabolic Syndrome ◽  
Obese Zucker Rat ◽  
Oxide Synthase ◽  
Wild Blueberry

This study evaluates the effect of wild blueberry (WB) consumption on the biomechanical properties of the aorta in the obese Zucker rat (OZR), a model of the metabolic syndrome. Thirty-six OZRs and 36 lean controls (lean Zucker rats) were placed either on a WB-enriched or a control (C) diet for 8 weeks. Phenylephrine (Phe)-mediated vasoconstriction and acetylcholine (Ach)-mediated vasorelaxation in the aortic vessel were investigated, as well as the contribution of the nitric oxide synthase and cyclooxygenase (COX) pathways in each of the above responses by using specific inhibitors. Obese Zucker rats exhibited a reduced vasocontstrictor response to Phe and an exaggerated vasorelaxant response to Ach. The WB diet partially restored Phe-induced constrictor responses and attenuated Ach-induced relaxant responses in OZR. Plasma nitric oxide was significantly attenuated (22.1 ± 1.1 μmol·L−1, WB vs 25.6 ± 1.4 μmol·L−1, C, p ≤ 0.05) with the WB diet. Thromboxane A2 levels in the aortic effluent were not significantly affected in the WB diet group, while PGI2 concentration significantly increased (766.5 ± 92.2 pg·mg−1 aorta in the WB vs 571.7 ± 37.8 pg·g−1 aorta in the C group, p ≤ 0.05). Downregulation of inducible nitric oxide synthase and COX2 expression in the OZR aorta was observed in the WB diet group. In conclusion, WB consumption altered the biomechanical properties of the OZR aorta by partially restoring the impaired Phe-induced constrictor responses and attenuating the exaggerated response to Ach-induced vasorelaxation.

Sitagliptin Attenuates Endothelial Dysfunction of Zucker Diabetic Fatty Rats: Implication of the Antiperoxynitrite and Autophagy

2017 ◽  
Vol 23 (1) ◽  
pp. 66-78 ◽  
Author(s):  
Huanyuan Wang ◽  
Yi Zhou ◽  
Zhiying Guo ◽  
Yu Dong ◽  
Jiahui Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Mesenteric Arteries ◽  
Zucker Rats ◽  
Protective Effects ◽  
Zucker Diabetic Fatty Rats ◽  
Zdf Rats ◽  
Oxide Synthase ◽  
Endothelium Dependent Relaxation

Although the contributions of sitagliptin to endothelial function in diabetes mellitus were previously reported, the potential mechanisms still remain undefined. Our research was intended to explore the underlying mechanisms of protective effects of sitagliptin treatment on endothelial dysfunction in Zucker diabetic fatty (ZDF) rats. Male lean nondiabetic Zucker rats were used as control and male obese ZDF rats were randomly divided into ZDF and ZDF + sitagliptin groups. The significant decrease in endothelium-dependent relaxation induced by acetylcholine was observed in mesenteric arteries and thoracic aorta rings of ZDF rats. The administration of sitagliptin restored the vascular function effectively. The morphology study showed severe endothelial injuries in thoracic aortas of ZDF rats, and sitagliptin treatment attenuated these changes. The increased malondialdehyde levels and decreased superoxide dismutase activities in serum of ZDF rats were reversed by sitagliptin treatment. Sitagliptin also increased the expression of endothelial nitric oxide synthase and microtubule-associated protein 1 light chain 3 (LC3) and decreased the expression of inducible nitric oxide synthase, 3-nitrotyrosine, and p62 in ZDF rats. After giving Fe (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride porphyrin pentachloride (FeTMPyP, a peroxynitrite [ONOO−] scavenger) or sitagliptin to high-glucose (30 mmol/L, 48 hours) cultured human umbilical vein endothelial cells (HUVECs), the increased levels of Beclin-1 and lysosome-associated membrane protein type 2 were detected. Both FeTMPyP and sitagliptin also significantly increased the number of mRFP-GFP-LC3 dots per cell, suggesting that autophagic flux was increased in HUVECs. Our study indicated that sitagliptin treatment can improve the endothelium-dependent relaxation and attenuate the endothelial impairment of ZDF rats. The protective effects of sitagliptin are possibly related to antiperoxynitrite and promoting autophagy.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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