Endothelium-dependent and independent vasodilation studied at normoglycaemia in Type I diabetes mellitus with and without microalbuminuria

Dogra, Gursharan; Rich, Lisa; Stanton, K.; Watts, Gerald F.

doi:10.1007/s001250051665

Cited by 135 publications

(108 citation statements)

References 34 publications

(43 reference statements)

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“…The slightly more pronounced impairment of glomerular hemodynamics in type 2 diabetic patients with microangiopathy may suggest that the defect of NO regulation of glomerular function worsens progressively with the occurrence of renal complications. These findings are in keeping with the observations of Dogra et al (38) who have shown that endothelial dysfunction is present in normoalbuminuric type 1 diabetic patients, and is more marked in microalbuminurics.…”

Section: Discussionsupporting

confidence: 93%

Nitric oxide modulation of renal and cardiac hemodynamics in type 2 diabetes

Vestra

Sacerdoti²,

Bombonato³

et al. 2002

European Journal of Endocrinology

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Objective: To evaluate endothelial function in type 2 diabetic patients with and without diabetic nephropathy. Methods: We studied the effects of systemic infusion of the nitric oxide (NO) synthase inhibitor N Gmonomethyl-L-arginine (L-NMMA) on cardiovascular and renal hemodynamics in six type 2 diabetic patients with microalbuminuria (D2-MA), six type 2 diabetic patients with normoalbuminuria (D2-NA) and five control subjects. Both type 2 diabetic patients and control subjects had mild arterial hypertension. Results: L-NMMA infusion decreased the cardiac index in all groups. A reduction in glomerular filtration rate (GFR) and an increase in filtration fraction were observed only in controls. Renal plasma flow decreased in controls and D2-NA patients and renal vascular resistance increased in all groups. Conclusions: The effect of L-NMMA on cardiac output was similar in controls and type 2 diabetic patients with and without diabetic nephropathy. In contrast, the effect on GFR was impaired in both diabetic groups, suggesting that glomerular NO homeostasis is altered in type 2 diabetes. Moreover the discrepancy, in diabetic patients, between cardiac and renal effects during L-NMMA infusion suggests that the modulation of glomerular hemodynamics is independent from NO-regulated cardiac output.

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Section: Discussionsupporting

confidence: 93%

Nitric oxide modulation of renal and cardiac hemodynamics in type 2 diabetes

Vestra

Sacerdoti²,

Bombonato³

et al. 2002

European Journal of Endocrinology

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“…36 The finding of an inverse association between UACR and NMD indicates that increased urinary albumin excretion in hypertensive subjects may be a marker of arterial smooth muscle hyporeactivity to exogenous sources of NO. Several previous studies 27,28,31,37 have reported significantly lower NMD in microalbuminuric than in normoalbuminuric patients; however, the subjects in these studies were mostly normotensive diabetics and non-diabetics. Vasodilatation owing to nitroglycerin involves Abbreviations: BMI, body mass index; DBP, diastolic blood pressure; FMD, flow-mediated dilatation; HDL, high-density lipoprotein; SBP, systolic blood pressure; UACR, urinary albumin/creatinine ratio.…”

Section: Discussionmentioning

confidence: 82%

“…As FMD primarily results from the endothelial release of nitric oxide (NO), 26 the inverse association between UACR and FMD indicates that increased urinary albumin excretion in hypertensive individuals may be a manifestation of systemic endothelial dysfunction. Previous studies investigating the relationship between urinary albumin excretion and FMD have yielded conflicting results, with some showing a significant association [27][28][29][30][31] and others showing no such association. [32][33][34] The reasons for these divergent observations are not clear, although methodological differences between various studies could contribute.…”

Section: Discussionmentioning

confidence: 97%

Urinary albumin excretion is associated with impaired flow- and nitroglycerin-mediated brachial artery dilatation in hypertensive adults

et al. 2007

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We investigated whether the urinary albumin/creatinine ratio (UACR), a measure of albuminuria, is associated with non-invasive measures of arterial function in hypertensive adults without known coronary heart disease (CHD) or stroke. UACR was measured in the first voided morning urine sample in 469 non-Hispanic white hypertensive individuals (mean age 62.279.8 years, 41% men) belonging to hypertensive sibships. High-resolution ultrasonography of the brachial artery was used to assess flow-mediated dilatation (FMD) -an endothelium-dependent response -and nitroglycerin-mediated dilatation (NMD) -an endothelium-independent response. Because of skewed distribution, UACR was log transformed after addition of 0.1. The association of log (UACR þ 0.1) with FMD and NMD, before and after adjustment for CHD risk factors, serum creatinine, and hypertension medication and statin use was assessed using linear regression analyses. In univariable analyses, variables associated with lower FMD were greater age, male sex, history of smoking, lower high-density lipoprotein (HDL) cholesterol, higher serum creatinine and higher log (UACR þ 0.1); variables associated with lower NMD were greater age, male sex, higher systolic blood pressure, lower HDL cholesterol, higher serum creatinine and higher log (UACR þ 0.1). In separate stepwise multivariable regression analyses that adjusted for conventional CHD risk factors, serum creatinine and hypertension medication and statin use, higher log (UACR þ 0.1) was associated with lower brachial artery FMD (P ¼ 0.035) and NMD (P ¼ 0.0002). These findings highlight the association of increased urinary albumin excretion with impaired vascular reactivity in hypertensive individuals.

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“…Brachial artery ultrasonography was carried out [28]. Briefly, a 12-megahertz transducer connected to an Acuson Aspen ultrasound (Acuson, Mountain View, Calif, USA) and fixed in position by a stereotactic clamp 5 to 10 cm proximal to the ante-cubital crease was used to image the brachial artery.…”

Section: Methodsmentioning

confidence: 99%

Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

et al. 2002

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In Type II (non-insulin-dependent) diabetes mellitus the pathogenesis of vascular disease, its most common complication, remains unclear [1]. Endothelial dysfunction reflects the disordered physiology of several endothelium-derived vasoactive factors, in particular nitric oxide [2]. Endothelial dysfunction occurs commonly in diabetes and is an early feature of vasculopathy [3,4]. Increased oxidative stress due to the effects of hyperglycaemia and its sequelae is a recognized feature of diabetes [5]. It might cause endothelial dysfunction through the inactivation and Abstract Aim/hypothesis. We assessed whether dietary supplementation with coenzyme Q 10 improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia. Methods. A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q 10 or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flowmediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F 2 -isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity. Results. The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q 10 and decreased by ±0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q 10 treatment resulted in a threefold increase in plasma coenzyme Q 10 (p < 0.001) but did not alter plasma F 2 -isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure. Conclusion/interpretation. Coenzyme Q 10 supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F 2 -isoprostane concentrations. [Diabetologia (2002) 45: 420±426]

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Endothelium-dependent and independent vasodilation studied at normoglycaemia in Type I diabetes mellitus with and without microalbuminuria

Cited by 135 publications

References 34 publications

Nitric oxide modulation of renal and cardiac hemodynamics in type 2 diabetes

Nitric oxide modulation of renal and cardiac hemodynamics in type 2 diabetes

Urinary albumin excretion is associated with impaired flow- and nitroglycerin-mediated brachial artery dilatation in hypertensive adults

Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

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