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PubMed1998

Interaction between superoxide anion and nitric oxide in the regulation of vascular endothelial function.

1. Nitric oxide (NO)-mediated, endothelium-dependent vasodilator function in rat aortic smooth muscle was investigated in an in vitro model of endogenous vascular superoxide anion stress, generated by pretreatment with the Cu/Zn superoxide dismutase (SOD, EC 1.15.1.1) inhibitor, diethyldithiocarbamate (DETCA). 2. Contraction to noradrenaline (NA, 1 nM - 1 microM) in endothelium-intact vessels was augmented after a 30 min pretreatment with DETCA (10 mM) followed by 30 min washout. This effect was abolished by N(G)-nitro-L-arginine methyl ester (L-NAME, 0.3 mM) and removal of the endothelium and partially reversed by exogenous Cu/Zn SOD (200 u ml(-1)). 3. Endothelium- and basal NO-dependent vasorelaxation to the phosphodiesterase (PDE) type V inhibitor ONO- 1 505 (4-[2-(2-hydroxyethoxy)ethylamino]-2-(1H-imidazol-1-yl)-6-methoxyquin azoline methanesulphonate) (0.1-10 microM) was inhibited after DETCA (10 mM) pretreatment. In addition, the ability of L-NAME (0.3 mM) to enhance established contractile tone was effectively absent. 4. In contrast, DETCA pretreatment did not significantly affect vasorelaxation to acetylcholine (ACh, 1 nM - 3 microM) or S-nitroso-N-acetyl penicillamine (SNAP, 0.03-30 microM). However, L-NAME (0.3 mM) unmasked an inhibitory effect of DETCA pretreatment on vasorelaxation to SNAP in endothelium-intact vessels while markedly potentiating vasorelaxation to SNAP in control tissue. 5. L-NAME (0.3 mM)- and exogenous catalase (200 u ml(-1))-sensitive vasorelaxation to exogenous Cu/ Zn SOD (200 u ml(-1)) was greater after DETCA (10 mM) pretreatment in endothelium-intact aortic rings. This difference was abolished by catalase (200 u ml(-1)). 6. In conclusion, tissue Cu/Zn SOD inhibition elicited a selective lesion in basal endothelial function in rat isolated aortic smooth muscle, consistent with the inactivation of basal NO by superoxide anion. The resulting leftward shift in nitrovasodilator reactivity, due to the loss of the tonic depression by basal NO, is likely to mask the inhibitory effect of superoxide anion on agonist-stimulated endothelial function and nitrovasodilator-derived NO, thereby accounting for the differential pattern of endothelial dysfunction after DETCA pretreatment.

Animals↗

PubMed2002

Brachial endothelial function is impaired in patients with systemic lupus erythematosus.

OBJECTIVE: To verify if endothelial function is impaired in pre-menopausal women with systemic lupus erythematosus (SLE) and whether endothelial dysfunction is related to disease duration, cumulative prednisone dose, antimalarial use, anticardiolipin antibody (aCL), hypertension, Raynaud's phenomenon, disease activity score, and vasculitis. METHODS: Using high-resolution ultrasound, we measured the diameter of brachial artery at rest, during reactive hyperemia, and after glyceryl trinitrate (GTN). We compared 69 pre-menopausal female patients with SLE (mean age 29 +/- 8 years) with 35 age and sex-matched controls (mean age 29 +/- 6 years), The mean disease duration was 72 months. RESULTS: There was no significant difference in baseline brachial artery diameter. The flow-mediated dilation (endothelial dependent dilation) was significantly impaired in SLE patients when compared to controls (5.0 +/- 5.0% vs 12.0 +/- 6.0%, p < 0.001), even in the subgroup of patients without coronary artery disease risk factor (4.5 +/- 4.0% vs 12.0 +/- 6.0%, p < 0.001). The GTN induced dilation (endothelial independent dilation) was significantly lower in the aCL positive SLE patients when compared to the controls (11.9 +/- 4.0% vs 16.3 +/- 6.0%, p < 0.05). The endothelium-dependent dilation was not related to disease duration, cumulative prednisone dose, antimalarial use, anticardiolipin antibody, hypertension history, Raynaud's phenomenon, SLE disease activity score or vasculitis. CONCLUSION: This is the first study using brachial artery ultrasound imaging to evaluate endothelium function in SLE. Patients with SLE presented lower flow mediated dilation (endothelium dependent dilation) than sex and age-matched controls, even in patients without traditional cardiovascular risk factors and this may represent an early atherosclerotic process.

Adult↗

PubMedDate not supplied

Dietary measures and exercise training contribute to improvement of endothelial function and atherosclerosis even in patients given intensive pharmacologic therapy.

PURPOSE: Atherosclerosis contributes to cardiovascular mortality and morbidity even with aggressive lipid management. Our objective is to determine whether a combined pharmacological and lifestyle intervention can improve atherosclerosis. METHODS: We conducted a 2-year observational study at a specialized clinic in a tertiary care hospital. One hundred fifty-six subjects with coronary disease were enrolled in an intensive pharmacological management and lifestyle measures (including counseling and exercise training) program designed to reach specific targets. The main outcome measures were carotid intima media thickness and plaque area; brachial artery flow-mediated dilation; nitroglycerin-mediated dilation; flow-mediated dilation-nitroglycerin-mediated dilation ratio; laboratory parameters including lipids, glucose, creatinine, and homocysteine; and physical fitness. RESULTS: At completion, there were improvements in lipids and physical fitness. There were no overall changes in flow-mediated dilation, nitroglycerin-mediated dilation, or carotid intima media thickness in the entire cohort. However, multivariate logistic regression showed that dietary and exercise variables, such as increasing fiber intake and reducing body weight and body fat percentage, were independent predictors of improvements in endothelial function and carotid plaque burden. CONCLUSIONS: Even in the setting of intensive pharmacological therapy, lifestyle interventions, including exercise training and dietary changes, are important determinants of improved endothelial function and atherosclerosis.

Analysis of Variance↗

PubMed2006

Daily consumption for six weeks of a lignan complex isolated from flaxseed does not affect endothelial function in healthy postmenopausal women.

The occurrence of menopause is associated with an increased risk of cardiovascular events, and this has partly been attributed to the decline in circulating levels of estrogen. A lignan complex rich in the plant lignan secoisolariciresinol diglucoside (SDG) was isolated from flaxseed. SDG is metabolized by the colonic microflora to the mammalian lignans enterodiol and enterolactone and is hypothesized to be cardioprotective due to their structural similarity to estrogen. The aim of this study was to investigate the effect of a lignan complex, providing 500 mg/d of SDG, on markers of endothelial function. Healthy postmenopausal women (n = 22) completed a randomized, double-blind, placebo-controlled, crossover study. Women consumed daily a low-fat muffin, with or without a lignan complex, for 6 wk, separated by a 6-wk washout period. Flow-mediated, endothelium-dependent vasodilatation (FMD) and nitroglycerine-mediated, endothelium-independent vasodilatation were measured at the end of each intervention period. The sum of Plasma nitrite and nitrate (NOx), endothelin-1 (ET-1), and asymmetric dimethylarginine (ADMA) were measured at the beginning and end of each intervention period. FMD was 3.6 +/- 0.9% (mean +/- SEM) after the lignan complex intervention period compared with 3.9 +/- 0.7% after the placebo period (P = 0.72). Plasma concentrations of NOx, ET-1, and ADMA were not affected. We conclude that daily consumption for 6 wk of a low-fat muffin enriched with a lignan complex had no effect on endothelial function in healthy postmenopausal women.

4-Butyrolactone↗

PubMed1991

Substance P for evaluation of coronary endothelial function after cardiac transplantation.

The endothelium-dependent vasodilator substance P dilates normal and diseased coronary vessels in humans in vivo and produces a maximal response similar to that seen with intracoronary isosorbide dinitrate. Twelve cardiac transplant recipients underwent intracoronary infusion of substance P after routine annual investigations. All patients were well, with no evidence of rejection and with angiographically normal coronary arteries. Substance P was infused at 2 ml/min for 2 min into the coronary artery, starting at a dose of 1.4 pmol/min and increasing by doubling increments, and followed by isosorbide dinitrate (1 mg/min) infused over 2 min. Coronary artery diameter was measured in 23 vessel segments from 12 transplant recipients. The following doses were infused: saline solution (1 ml/min), substance P (0.7 [three patients], 1.4, 2.8, 5.6, 11.2, 22.4 pmol/min) and isosorbide dinitrate (1 mg/min). The mean percent increase in diameter (+/- SEM) in response to increasing doses of substance P was as follows: 0, 6.5 +/- 2.9%, 10.9 +/- 2.9%, 12.1 +/- 2.9%, 16.5 +/- 2.6%, 19.2 +/- 3.1% and 25.8 +/- 2.2%, respectively. Half maximal dilation was produced with 1.4 to 2.8 pmol/min of substance P; the maximal response (mean percent diameter change) was 22 +/- 2.5%. This was not significantly different from that achieved with isosorbide dinitrate. It is concluded that coronary endothelial function as assessed by response to substance P is preserved in cardiac transplant recipients with angiographically normal coronary arteries. Substance P may be a suitable agent for testing endothelial function in these patients.

Coronary Angiography↗

PubMed2002

Adverse effects of nitroglycerin treatment on endothelial function, vascular nitrotyrosine levels and cGMP-dependent protein kinase activity in hyperlipidemic Watanabe rabbits.

OBJECTIVE: With the present studies we sought to determine how treatment with nitroglycerin (NTG) affects endothelial function, oxidative stress and nitric oxide (NO)-downstream signaling in Watanabe heritable hyperlipidemic rabbits (WHHL). BACKGROUND: In vitro experiments have demonstrated potent antiatherosclerotic effects of NO suggesting that treatment with NO-donors such as NTG could compensate for the diminished availability of endothelial NO. Nitric oxide may, however, not only be scavenged by reaction with endothelium-derived superoxide but also form the potent oxidant and inhibitor of vascular function, peroxynitrite (ONOO(-)). METHODS: Watanabe heritable hyperlipidemic rabbits were treated for three days with NTG patches. Normolipidemic New Zealand White rabbits (NZWR) served as controls. Endothelial function was assessed ex vivo with organ chamber experiments and vascular superoxide was quantified using lucigenin (5 and 250 microM) and CLA-enhanced chemiluminescence. Vascular ONOO(-) formation was determined using nitrotyrosine antibodies. The activity of the cGMP-dependent kinase (cGK-I) was assessed by determining the phosphorylation of vasodilator-stimulated phosphoprotein VASP (P-VASP). RESULTS: Nitroglycerin treatment caused endothelial dysfunction in NZWR and WHHL, associated with an increase in superoxide and ONOO(-) production and a substantial drop in cGK-I activity. In vivo NTG-treatment decreased lipophilic antioxidants (alpha- and beta-carotene) in NZWR and WHHL. Treatment of NZWR with NTG also decreased plasma extracellular superoxide dismutase (EC-SOD)-activity. CONCLUSIONS: Nitroglycerin treatment of WHHL with exogenous NO worsens rather than improves endothelial dysfunction secondary to increased formation of superoxide and/or peroxynitrite leading to decreased cGK-I activity. The decrease in plasma levels of alpha- and beta-carotene may be at least in part due to a decrease in EC-SOD activity.

Animals↗

PubMed1995

Comparison of endothelial function between in situ and reversed vein graft: differences in endothelium-dependent responses.

BACKGROUND: The endothelium releases endothelium-derived relaxing factors that are potent vasodilators and inhibitors of platelet aggregation. Experiments were performed to determine whether the endothelium-dependent responses differed between in situ and reversed vein grafts. The influence of valve disruption or of dissection of the adventitia was also examined. METHODS: Segments of canine jugular veins were grafted into the carotid arteries during procedures such as reversed grafting, in situ grafting with valve disruption, in situ grafting without valve disruption, and in situ grafting with dissection of adventitia. After 4 weeks the endothelium-dependent responses of the grafts were examined by isometric tension recording. RESULTS: In the reversed and in situ vein graft with valve disruption, acetylcholine caused endothelium-independent contractions, whereas in the in situ vein graft without valve disruption acetylcholine-induced endothelium-dependent relaxations were preserved. Adenosine diphosphate (ADP) caused comparable endothelium-dependent relaxations in the in situ vein graft irrespective of valve disruption. In the reversed vein graft ADP-induced relaxations were significantly impaired. In the in situ vein graft with dissection of the adventitia, relaxations in response to acetylcholine and ADP were significantly reduced. CONCLUSIONS: These results suggest that endothelial function, in terms of endothelium-derived relaxing factors in the in situ vein graft, can be preserved and that adventitial dissection in the in situ vein graft should be minimized to preserve endothelial function.

Acetylcholine↗

PubMed2002

Effects of ethinyl estradiol, estradiol, and testosterone on hindlimb endothelial function in vivo.

SUMMARY: This study was designed to evaluate the effects of chronic treatment with estrogen and testosterone on hindlimb vascular function. Spontaneously hypertensive rats (SHR) were sham-operated (SHAM) or ovariectomized and treated with vehicle (OVX), ethinyl estradiol (OVX-EE2), estradiol (OVX-E2), or testosterone (OVX-TESTO) for 3 weeks. Anesthetized SHR were instrumented for the measurement of arterial blood pressure and hindlimb blood flow. Ovariectomy had no significant effect on hindlimb resistance. Resting blood pressure (mm Hg) and hindlimb resistance (mm Hg/ml/min/kg) were higher in OVX-TESTO (158 +/- 4 and 4.7 +/- 0.3) than SHAM control (130 +/- 6 and 3.3 +/- 0.4), OVX (139 +/- 6 and 3.4 +/- 0.3), OVX-EE2 (130 +/- 4 and 3.0 +/- 0.3), and OVX-E2 (120 +/- 4 and 3.3 +/- 0.4). The hemodynamic responses to the endothelium-dependent vasodilator acetylcholine (ACh) were similar in SHAM, OVX, OVX-EE2, and OVX-E2. The hindlimb vasodilatory effects of ACh were consistently greater in OVX-TESTO compared with OVX, OVX-EE2, OVX-E2, and SHAM control rats. The hemodynamic responses to the nitric oxide donor, sodium nitroprusside, were similar in all groups. Our results provide evidence of modulatory influence of testosterone on vasomotor function. It is suggested that the enhanced hindlimb endothelial function represents a compensatory mechanism for testosterone-induced hypertension.

Animals↗

PubMed1998

Regulation of the actin cytoskeleton by thrombin in human endothelial cells: role of Rho proteins in endothelial barrier function.

Endothelial barrier function is regulated at the cellular level by cytoskeletal-dependent anchoring and retracting forces. In the present study we have examined the signal transduction pathways underlying agonist-stimulated reorganization of the actin cytoskeleton in human umbilical vein endothelial cells. Receptor activation by thrombin, or the thrombin receptor (proteinase-activated receptor 1) agonist peptide, leads to an early increase in stress fiber formation followed by cortical actin accumulation and cell rounding. Selective inhibition of thrombin-stimulated signaling systems, including Gi/o (pertussis toxin sensitive), p42/p44, and p38 MAP kinase cascades, Src family kinases, PI-3 kinase, or S6 kinase pathways had no effect on the thrombin response. In contrast, staurosporine and KT5926, an inhibitor of myosin light chain kinase, effectively blocked thrombin-induced cell rounding and retraction. The contribution of Rho to these effects was analyzed by using bacterial toxins that either activate or inhibit the GTPase. Escherichia coli cytotoxic necrotizing factor 1, an activator of Rho, induced the appearance of dense actin cables across cells without perturbing monolayer integrity. Accordingly, lysophosphatidic acid, an activator of Rho-dependent stress fiber formation in fibroblasts, led to reorganization of polymerized actin into stress fibers but failed to induce cell rounding. Inhibition of Rho with Clostridium botulinum exoenzyme C3 fused to the B fragment of diphtheria toxin caused loss of stress fibers with only partial attenuation of thrombin-induced cell rounding. The implication of Rac and Cdc42 was analyzed in transient transfection experiments using either constitutively active (V12) or dominant-interfering (N17) mutants. Expression of RacV12 mimicked the effect of thrombin on cell rounding, and RacN17 blocked the response to thrombin, whereas Cdc42 mutants were without effect. These observations suggest that Rho is involved in the maintenance of endothelial barrier function and Rac participates in cytoskeletal remodeling by thrombin in human umbilical vein endothelial cells.

Actins↗

PubMed2002

Association between increased iron stores and impaired endothelial function in patients with hereditary hemochromatosis.

OBJECTIVES: We studied associations between iron status and early functional and structural vascular abnormalities in patients with hereditary hemochromatosis (HH). BACKGROUND: Iron may be involved in atherogenesis, and patients bearing a genetic mutation associated with HH are possibly at risk of developing coronary heart disease. METHODS: We studied the vascular properties of 41 HH patients who had homozygosity for the C282Y mutation, along with 51 age-matched control subjects, by determination of endothelium-dependent dilation (EDD) of the brachial artery and intima-media thickness (IMT) of the carotid artery. RESULTS: Male HH patients who were not receiving phlebotomy therapy showed a reduced EDD and increased IMT compared with controls and HH patients receiving therapy. In female HH patients, irrespective of treatment status, vascular parameters were not different from those of controls, and none of these patients had severe iron overload. In HH patients, increased iron load was significantly associated with reduced EDD and increased IMT. Moreover, we found a positive correlation between body iron stores and indicators of oxidative stress. When previously untreated male HH patients were re-investigated after intensive phlebotomy therapy, a significant improvement in EDD was observed (2.6 +/- 1.3% before vs. 5.5 +/- 2.1% after treatment, p = 0.0015). CONCLUSIONS: Impaired endothelial function and increased IMT are associated with iron overload, with subsequent induction of oxidative stress, and are not linked to a genetic disability in HH patients. Consequent iron-depletion therapy normalizes endothelial function and may thus reduce the increased risk of cardiovascular events. Female patients may be at a reduced risk, presumably due to continuous iron loss by menstruation.

Adult↗

PubMed2002

Simvastatin improves endothelial function in spontaneously hypertensive rats through a superoxide dismutase mediated antioxidant effect.

BACKGROUND: Hydroxymethylglutaryl coenzyme A (HMGCoA) reductase inhibitors have beneficial effects beyond their cholesterol-lowering properties. The antioxidant mechanism of HMGCoA reductase inhibitors is not completely understood. OBJECTIVES: To elucidate the antioxidant effect of simvastatin. METHODS: We studied the influence of simvastatin treatment on the development of hypertension, modification of antioxidant systems, and reactivity of aortic rings in Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. RESULTS: Simvastatin had no effect on blood pressure (BP). Simvastatin treatment (either 1 or 2 mg/kg body weight for 12 or 20 weeks) increased superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in SHR rats compared with untreated control SHR rats. Carbachol-induced relaxation of aortic rings was impaired in control SHR rats and was restored by simvastatin treatment. Addition of SOD improved the response in control SHR rats and did not have any effect in treated SHR rats. Addition of diethyldithiocarbamic acid, a selective inhibitor of SOD, produced a mild non-significant impairment in carbachol-induced relaxation in control SHR rats, suggesting a deficient antioxidant system in these animals. However, in treated SHR and in WKY rats, impairment of the relaxation was marked, implying that SOD activity in these animals was important to maintain endothelial function. In aortic rings without endothelium from SHR rats, contraction induced by free radicals was substantially higher than in WKY rats. This effect was attenuated in 1-mg-treated rats and abolished in 2-mg-treated rats. CONCLUSIONS: Simvastatin promotes intracellular antioxidant systems, fundamentally SOD, restoring endothelial function but not having any effect on blood pressure.

Animals↗

PubMed2007

Effects of cardioversion of atrial fibrillation on endothelial function in hypertension or diabetes.

BACKGROUND: Cardioversion (CV) to sinus rhythm corrects endothelial dysfunction secondary to atrial fibrillation (AF). As AF often complicates hypertension and diabetes (disorders associated with impaired endothelial function) the study probed whether these comorbidities to AF produced an additive effect and to what extent CV might be advantageous. MATERIALS AND METHODS: Brachial artery flow-mediated dilatation (FMD) was evaluated before and after CV in 17 lone AF patients (group 1), 16 patients with AF + hypertension (group 2) and 17 patients with AF + diabetes type II (group 3), while in supine and head-up tilting (HUT) positions, as this is when endothelial vasodilation is emphasized as a counterbalance to neurogenic vasoconstriction. RESULTS: After 2 weeks, CV in group 1 increased (P < 0.01) supine FMD (from 7.22-->9.50%) and restored its HUT potentiation (from 9.31-->17.22%). In group 2, FMD also improved significantly with CV (supine from 4.92-->7.11% and HUT from 5.29-->11.83%; P < 0.01). In group 3, CV did not promote significant FMD changes (supine from 5.12-->4.92% and HUT from 4.98-->4.73%). After 3 months, FMD improvement persisted in groups 1 and 2 with enduring sinus rhythm, but not in those with AF relapse. In group 3, FMD remained unchanged regardless of cardiac rhythm. CONCLUSIONS: Cardioversion persistently increases supine shear stress endothelial responsiveness and restores the orthostatic modulation in AF alone or in association with hypertension, but not with diabetes. Differences in background endothelial impairment may explain the presence (hypertension) or the absence (diabetes) of an additive AF effect in comorbidities, as well as CV results.

Atrial Fibrillation↗

PubMed2003

Endothelial function and menopause: effects of raloxifene administration.

Postmenopausal women have more severe endothelial dysfunction than premenopausal women. In the present study, we evaluated the possible beneficial effect of raloxifene administration, a selective estrogen receptor modulator, on endothelial regulation in postmenopausal women. In a double-blind, randomized vs. placebo trial, 60 healthy postmenopausal women were treated with raloxifene (60 mg/d) or placebo for 4 months to evaluate the effect of raloxifene treatment on endothelial function. Furthermore, in raloxifene-treated subjects (n = 30), the effect of raloxifene was also assessed during the intraarterial infusion of N(G)-monomethyl-L-arginine (4 micromol/min). Raloxifene administration vs. placebo was associated with a decrease in plasma low-density lipoprotein cholesterol (P < 0.01), triglyceride (P < 0.05), thiobarbituric acid-reactive substance (P < 0.01), vascular cell adhesion molecule-1 (P < 0.05), intercellular adhesion molecule-1 (P < 0.001), and E-selectin (P < 0.001) levels and with an increase in plasma Trolox equivalent antioxidant capacity (P < 0.001) levels. Indeed, raloxifene treatment was also associated with a significant improvement in endothelial-dependent vasodilatation assessed by brachial reactivity technique. Raloxifene administration had no impact on endothelial-independent vasodilatation. Furthermore, intraarterial infusion of N(G)-monomethyl-L-arginine inhibited the significant effect of raloxifene on endothelium-mediated brachial arterial diameter and flow. In conclusion, our results demonstrate that raloxifene administration is associated with a positive modulation of endothelial-dependent vasodilatation likely due to a reduction of risk factors for endothelial damage.

Adult↗

PubMedDate not supplied

Endothelial function evaluated by flow-mediated dilatation in pediatric vascular disease.

The endothelial function of children with and without vascular disease, consisting of 41 controls, 24 with Kawasaki disease (KD), and 46 with diabetes mellitus (DM), was examined. Age at examination ranged from 3 to 23 years (mean, 12.0 +/- 4.7). The flow-mediated dilatation (FMD) and intima-media complex in the common carotid artery were measured. In controls age at examination was not associated with FMD or intima-media complex. FMD significantly decreased in children with KD and DM compared with the control group (control vs KD or DM: 11.7 +/- 14.7 vs 3.0 +/- 11.0 or 6.4 +/- 8.5%, respectively; p < 0.05). However, there was no significant difference for intima-media complex among the groups. Furthermore, FMD in KD patients with coronary arterial aneurysm was lower than that in KD patients without aneurysm (-0.5 +/- 9.2 vs 8.3 +/- 9.1%, p < 0.05). In DM patients, FMD in the high HbA1c group (HbA1c = 7%) was lower than that in the normal HbA1c group (HbA1c < 7%) (4.8 +/- 8.1 vs 11.4 +/- 7.8%, p < 0.05). In conclusion, FMD detected endothelial impairment in children with KD or type 1 DM regardless of overt vascular complications, and FMD impairment occurs prior to intima-media complex thickening. By measuring both FMD and intima-media complex, useful information for predicting vascular complications may be obtained.

Adolescent↗

PubMed1999

Plasma polyphenols and antioxidants, oxidative DNA damage and endothelial function in a diet and wine intervention study in humans.

An intervention study was performed to evaluate the influence of a Mediterranean diet, a high fat diet, and their supplementation with red wine in moderate amounts, on biochemical, physiological, and clinical parameters related to atherosclerosis and other chronic diseases. For 3 months two groups of 21 male volunteers each, received either a Mediterranean diet or a high fat diet; during the second month, red wine was added isocalorically, 240 ml/day. Participants were kept under close medical and nutritional surveillance. At days 0, 30, 60 and 90, clinical, physiological and biochemical evaluations were made. Plasma vitamin C was significantly decreased in the high fat diet group compared to the Mediterranean diet group. After wine supplementation to the Mediterranean diet, a significant 13.5% increase in plasma vitamin C was observed. Furthermore, when wine was added vitamin E decreased significantly in plasma, 15% in the high fat diet and 26% in the Mediterranean diet. Total plasma antioxidant capacity (total antioxidant reactivity) increased 28% above basal levels in the Mediterranean diet group, but not in the high fat diet group. In both groups, wine induced a marked increase in total antioxidant reactivity above basal levels, 56% and 23%, respectively. Oxidative DNA damage, detected as 8-hydroxydeoxyguanosine (8-OHdG) levels in blood leukocyte DNA, was markedly increased by the high fat diet; however, it was strongly reduced, to approximately 50% basal values, after wine supplementation, both in the high fat diet and Mediterranean diet groups. Endothelial function, evaluated noninvasively as flow-mediated vascular reactivity of the brachial artery, was suppressed by the high fat diet, and was normal after wine supplementation. These effects are attributed to oxidative stress associated with a high fat diet, and to the elevated plasma antioxidant capacity associated with wine consumption and the Mediterranean diet. The results presented support the following conclusions: a high fat diet induces oxidative stress; a diet rich in fruits and vegetables enhances antioxidant defenses; wine supplementation to a high fat or a Mediterranean diet increases plasma antioxidant capacity, decreases oxidative DNA damage, and normalizes endothelial function.

Adult↗

PubMed1992

Uptake of polyamines by human endothelial cells. Characterization and lack of effect of agonists of endothelial function.

Uptake of polyamines by confluent monolayers of human umbilical-vein endothelial cells (HUVECs) was found to be time-, temperature- and concentration-dependent, energy-requiring, and saturable. Kinetic constants were putrescine Kt 3 +/- 1 microM, Vmax. 15 +/- 7 pmol/h per microgram of protein; spermidine, 0.7 +/- 0.2, 12 +/- 3; spermine, 1 +/- 0.7, 11 +/- 4. Putrescine uptake was inhibited by spermine or spermidine, whereas uptake of spermine or spermidine was not inhibited by 20 microM-putrescine. These data suggest the existence of two carriers, one shared by spermine and spermidine, and one capable of transporting all three polyamines. Pretreatment of HUVECs with thrombin (less than or equal to 10 units/ml; 1 h), bradykinin (less than or equal to 10 microM; 1 h), interleukin-1 (less than or equal to 100 units/ml; 2 h) or phorbol 12-myristate 13-acetate (less than or equal to 1.0 microM; 1 h), all known agonists of endothelial function, had no significant effect on polyamine uptake. These responses may be of importance in angiogenesis and wound healing, and could have pharmacological significance, for there is a growing interest in the use of polyamines or polyamine analogues as therapeutic agents.

2,4-Dinitrophenol↗

PubMed2003

Endothelial function is more impaired in hemodialysis patients than renal transplant recipients.

BACKGROUND: Endothelial dysfunction (ED) is a common precursor and denominator of cardiovascular events including development of atherosclerosis. In this cross-sectional, controlled study, we aimed to investigate ED measured by ischemia-induced forearm vasodilatation in chronic hemodialysis (HD) patients and renal transplant recipients (rTX). PATIENTS AND METHODS: Thirty-nine HD patients, 39 rTX and 38 normotensive healthy controls were included. There was no difference in age and gender distribution among the study groups. The mean time spent on dialysis and transplantation were 74 +/- 46 and 68 +/- 39 months. Serum high sensitive C-reactive protein (hs-CRP) and plasma fibrinogen levels were measured. Endothelium dependent post-ischemic vasodilatation of brachial artery was used to evaluate ED. RESULTS: The hs-CRP and plasma fibrinogen levels were significantly increased in HD patients when compared with rTX. On high resolution ultrasonographic examination, post-ischemic vasodilatation values in HD patients (9.55 +/- 6.47%) were significantly lower than rTX (14.39 +/- 8.06%, p = 0.007) and controls (20.42 +/- 6.10%, p < 0.001). Renal transplant recipients also had significantly lower post-ischemic vasodilatation values than controls (p = 0.001). The hs-CRP levels were negatively correlated with endothelium-dependent dilatations in TX (r = -0.59, p = 0.001), however, this correlation was not detected in HDp. CONCLUSION: Patients with end-stage renal disease have ED. Endothelial function is more impaired in HD patients than rTX. Different mechanisms might be responsible for ED in HD patients and rTX.

Adult↗

PubMed2003

[Real-time registration of flow-mediated dilatation for the assessment of endothelial function].

UNLABELLED: Flow-mediated dilatation (FMD) is used to qualify vascular endothelial function. AIM: To evaluate the feasibility of real-time assessment of the stimulus-to-response (i. e. flow-velocity-to-diameter) relationship, repeated FMD was assessed in healthy subjects. METHODS: Brachial artery diameter and flow velocity were measured simultaneously in 10 healthy male subjects lying in the supine position. These parameters were registered in real-time mode and beat-to-beat by means of a 7.5 MHz linear array transducer attached to a custom-built Wall Track System and an 8 MHz continuous wave Doppler. RESULTS: Post-ischaemic increase in arterial diameter amounted to 5.9 +/- 2.9 % with an average increase in blood flow velocity of 487 +/- 174 %. The relative change in diameter was not correlated to the relative increase in flow velocity. CONCLUSION: Continuous registration of FMD can be performed. Motion artefacts, however, interfere with the real-time registration of FMD.

Adult↗