Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation

Jin, Jong Shiaw; Bohlen, H. G.

doi:10.1152/ajpheart.1997.272.2.h728

Cited by 27 publications

(26 citation statements)

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“…22 Our observations are in agreement with previous studies demonstrating an endothelial dysfunction in obese Zucker rat, especially in the NO pathway. 20,23 An excessive ROS production might also cause this low NO bioavailability. This was evidenced by a rise in DHE staining and NADPH oxidase (gp91 and p67) expression in mesenteric arteries, as well as by the restoration of ACh-induced dilation by antioxidant treatments, as shown in Figure 3.…”

Section: Discussionmentioning

confidence: 99%

Flow-Induced Remodeling in Resistance Arteries From Obese Zucker Rats Is Associated With Endothelial Dysfunction

et al. 2007

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Abstract-Chronic increases in blood flow increase arterial diameter and NO-dependent dilation in resistance arteries.Because endothelial dysfunction accompanies metabolic syndrome, we hypothesized that flow-mediated remodeling might be impaired in obese rat resistance arteries. Obese and lean Zucker rat mesenteric resistance arteries were exposed to chronic flow increases through arterial ligation in vivo: arteries exposed to high flow were compared with normal flow arteries. Diameter was measured in vitro in cannulated arteries using pressure arteriography. After 7 days, outward remodeling (diameter increased from 346Ϯ9 to 412Ϯ11 m at 100 mm Hg) occurred in lean high-flow arteries. Endothelium-dependent tone was reduced in high-flow arteries from obese rats by contrast with lean animals. On the other hand, diameter enlargement occurred similarly in the 2 strains. The involvement of NO in endothelium-dependent dilation (evidenced by NO blockade) and endothelial NO synthase phosphorylation was smaller in obese than in lean rats. Superoxide anion and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunit expression (p67phox and gp91phox) increased in obese rats and were higher in high-flow than in control arteries. Acute Tempol (a catalase mimetic), catalase plus superoxide dismutase, and L-arginine plus tetrahydrobiopterin restored endothelium-dependent dilation in obese rat normal and high-flow arteries to the level found in lean control arteries. Thus, flow-induced remodeling in obese resistance arteries was associated with a reduced endothelium-mediated dilation because of a decreased NO bioavailability and an excessive superoxide production. This dysfunction might have negative consequences in ischemic diseases in patients with obesity or metabolic syndrome. Key Words: resistance arteries Ⅲ shear stress Ⅲ NO Ⅲ reactive oxygen species Ⅲ mechanotransduction Ⅲ obesity Ⅲ metabolic syndrome T he metabolic syndrome is a common health problem. Its incidence and prevalence are increasing in parallel with the enhanced prevalence and incidence of obesity and type 2 diabetes. 1,2 This syndrome is not only a metabolic disorder; it is also associated with endothelial dysfunction 3 and vascular remodeling leading to a reduction in arterial diameter. 4 Patients with metabolic syndrome demonstrate an increasing risk of overall mortality, as well as cardiovascular morbidity and mortality. 5 Basically, an increase in blood pressure or a decrease in blood flow induces a transient adjustment in vessel diameter mediated by changes in myogenic tone and by the release of vasoactive substances. On the other hand, increasing blood flow induces a vasodilation mediated by endothelium-derived NO. A long-term exposition to altered mechanical forces induces vascular remodeling to restore tensile and shear stresses. 6,7 Long-term increase in shear stress enhances NO production by endothelial cells, and we have shown previously that NO has a key role in vascular remodeling of large 8 and resistance arteries in response to an in...

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Section: Discussionmentioning

confidence: 99%

Flow-Induced Remodeling in Resistance Arteries From Obese Zucker Rats Is Associated With Endothelial Dysfunction

et al. 2007

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“…In contrast, a study by Andrews et al (Andrews et al, 2000) reports that vasodilation of the perfused hindquarter in response to acetylcholine was increased in diabetic obese Zucker rats when compared to lean Zucker rats. Others (Jin and Bohlen, 1997;Frisbee, 2001;Frisbee and Stepp, 2001), however, have shown selective impairment in nitric oxide synthasedependent dilation of peripheral blood vessels during type II diabetes mellitus. Jin and Bohlen (Jin and Bohlen, 1997) examined reactivity of intestinal arterioles in response to changes in blood flow and acetylcholine in lean and diabetic obese Zucker rats.…”

Section: Effects Of Type II Diabetes Mellitus On Responses Of Periphementioning

confidence: 99%

“…Others (Jin and Bohlen, 1997;Frisbee, 2001;Frisbee and Stepp, 2001), however, have shown selective impairment in nitric oxide synthasedependent dilation of peripheral blood vessels during type II diabetes mellitus. Jin and Bohlen (Jin and Bohlen, 1997) examined reactivity of intestinal arterioles in response to changes in blood flow and acetylcholine in lean and diabetic obese Zucker rats. These investigators found that flow-mediated and acetylcholine-induced dilation of intestinal arterioles were impaired in obese Zucker rats when compared to lean Zucker rats (Jin and Bohlen, 1997).…”

Section: Effects Of Type II Diabetes Mellitus On Responses Of Periphementioning

confidence: 99%

“…Jin and Bohlen (Jin and Bohlen, 1997) examined reactivity of intestinal arterioles in response to changes in blood flow and acetylcholine in lean and diabetic obese Zucker rats. These investigators found that flow-mediated and acetylcholine-induced dilation of intestinal arterioles were impaired in obese Zucker rats when compared to lean Zucker rats (Jin and Bohlen, 1997). Vasodilation in response to nitroprusside, however , was similar in lean and obese Zucker rats (Jin and Bohlen, 1997).…”

Section: Effects Of Type II Diabetes Mellitus On Responses Of Periphementioning

confidence: 99%

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Impaired nitric oxide synthase-dependent dilatation of cerebral arterioles in type II diabetic rats

Schwaninger

Sun

Mayhan³

2003

Life Sciences

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“…[10][11][12][13][14][15] However, human obesity primarily results from alterations in a combination of different genes (i.e., polygenic) that interact with environmental factors such as diet to promote aspects of the metabolic syndrome. Outbred Sprague-Dawley rats respond to a moderately high fat (MHF) diet with either an obesityprone (OP) or obesity-resistant (OR) phenotype.…”

Section: Introductionmentioning

confidence: 99%

Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

et al. 2006

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Objective: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. Design: Male Sprague-Dawley rats were fed either a low fat (LF; 11% kcal as fat) or a moderately high fat (MHF; 32% kcal as fat) diet for 11 weeks. Measurements: Body weight; mean arterial pressure; angiotensin peptides; mesenteric contractile response to phenylephrine (PE), potassium chloride (KCl), serotonin, angiotensin II (AngII), calcium chloride; baseline and isoproterenol-induced cardiac contractility; baseline and isoproterenol-induced coronary artery blood flow. Results: Rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups. OP rats exhibited elevations in mean arterial pressure (MAP) and elevations in systemic concentrations of angiotensin peptides. Mesenteric arteries from OP rats exhibited a greater contractile response to PE, KCl and serotonin (5-HT). Heightened responses to PE persisted in arteries from OP rats even after normalization of the response to KCl. In contrast, the response of permeabilized mesenteric arteries to a maximal concentration of calcium was similar in rats from each group. Isolated perfused hearts exhibited similar baseline and isoproterenol-induced contractility in rats from each group. However, isoproterenol was unable to increase coronary artery blood flow in hearts from OP rats. Conclusion: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand.

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Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation

Cited by 27 publications

References 0 publications

Flow-Induced Remodeling in Resistance Arteries From Obese Zucker Rats Is Associated With Endothelial Dysfunction

Flow-Induced Remodeling in Resistance Arteries From Obese Zucker Rats Is Associated With Endothelial Dysfunction

Impaired nitric oxide synthase-dependent dilatation of cerebral arterioles in type II diabetic rats

Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

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