Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Traupe, Tobias; d’Uscio, Livius V.; Muenter, Klaus; Morawietz, Henning; Vetter, W; Barton, Matthias

doi:10.1042/cs103s013s

Cited by 40 publications

(30 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…26 In C57BL/6 mice fed a high fat diet, the contractile response of the carotid artery to endothelin-1 was increased. 27 Similarly, a high fat diet resulted in obesity associated with an enhanced contractile response of the femoral artery to PE and norepinephrine. 28 These responses were not observed in mice fed the diet for 1 week, suggesting a role for obesity in enhanced vascular contractility.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2006

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2006

View full text Add to dashboard Cite

show abstract

“…10 Endothelin has also been reported to modulate endothelium-dependent vasoconstriction in obese mice fed a high-fat (HF) diet. 11 However, there has been no study, to our knowledge, that has addressed the importance of endothelin in mediating long-term increases in arterial pressure in dietary-induced obesity. Therefore, the main objective of this study was to determine whether endothelin-1 contributes to increased arterial pressure in rat a model of visceral obesity produced by a long-term HF diet.…”

mentioning

confidence: 99%

Role of Endothelin-1 in Blood Pressure Regulation in a Rat Model of Visceral Obesity and Hypertension

et al. 2004

View full text Add to dashboard Cite

Abstract-Endothelial dysfunction has been suggested to play an important role in the development of obesity-induced hypertension. Because endothelin release increases in response to endothelial damage, we examined whether endothelin-1 contributes to increased arterial pressure in a model of visceral obesity produced by feeding SpragueDawley rats a high-fat (HF) diet (40% fat w/w, nϭ6) for 12 months. Arterial and venous catheters were implanted for measurement of mean arterial pressure (MAP) and heart rate (HR) 24 hours per day and intravenous infusions. After a 5-day control period, rats were infused with the selective endothelin-1 type A receptor (ET-A) blocker ABT-627 (2.5 mg/kg per day, IV) for 9 days, followed by a recovery period. Rats fed a standard chow (normal fat, or NF, group: nϭ6) for 12 months were also infused with ET-A blocker and were used as controls. Compared with NF rats, HF rats had higher MAP (113Ϯ4 versus 98Ϯ2 mm Hg), increased visceral fat (18.7Ϯ2.0 versus 10.8Ϯ1.4 g), and 3.2-fold increase in plasma leptin despite similar total body weight gain. Long-term ET-A blockade markedly reduced MAP in HF (Ϫ14Ϯ3 mm Hg) and NF (Ϫ14Ϯ2 mm Hg), but it had no effect on HR, GFR, or PRA. These results indicate that a long-term HF diet may cause visceral obesity and increased MAP, even in the absence of major changes in total body weight. Endothelin-1 appears to play an important role in the maintenance of arterial pressure in rats fed HF and NF diets, but it does not appear to contribute to increased MAP in this model of diet-induced hypertension. Key Words: hypertension Ⅲ renin Ⅲ kidney Ⅲ diet Ⅲ obesity C onsiderable evidence suggest that excess weight gain is the most common cause of human essential hypertension. Risk estimates from the Framingham Heart Study, for example, indicate that Ϸ78% of hypertension in men and 65% in women can be directly attributed to obesity.

show abstract

“…These two changes weaken the protective role of the endothelium with reduced nitric oxide production and enhanced responsiveness to endothelin. 8,9,10 Summarizing these findings, Traupe et al advocate that obesity related increases in production of EDCFs may contribute to the development of vascular diseases. As insulin resistance advances and patients develop diabetes, comparable vascular abnormalities are present at the endothelial level 11,12 (see Figure 1).…”

Section: Pathobiology Of Atherosclerosismentioning

confidence: 99%

Effect of glitazones on the progression of coronary artery disease in type 2 diabetes patients

Chilton¹

2009

View full text Add to dashboard Cite

Abstract:The effect of thiazolidinediones (TZDs) on the progression of atherosclerosis in diabetes patients remains unclear. There has been heightened interest in recent years in this class of diabetes medications due to the non-glycemic lowering effects, such as altering lipids, inflammation and hematologic profiles. There have been several exciting studies over the past few years focused on the mechanism of action of the TZDs with respect to alteration in the cardio-metabolic profile in diabetes patients. New tools such as intravascular ultrasound have been used to follow plaques characteristics over time on a much more sensitive scale than has ever been possible in the past by coronary angiograms. These advances have enabled researchers to follow closely the macrovascular effects of different anti-atherosclerotic medications such as statins and TZDs. This article reviews the pathophysiology of atherosclerosis in diabetes, the role that TZDs play in this process and the imaging trials looking at the progression or regression of atherosclerosis in patients treated with TZDs.

show abstract

Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Cited by 40 publications

References 12 publications

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

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

Role of Endothelin-1 in Blood Pressure Regulation in a Rat Model of Visceral Obesity and Hypertension

Effect of glitazones on the progression of coronary artery disease in type 2 diabetes patients

Contact Info

Product

Resources

About