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PubMed2004

Impaired L-arginine transport and endothelial function in hypertensive and genetically predisposed normotensive subjects.

BACKGROUND: Impaired endothelium-dependent NO-mediated vasodilation is a key feature of essential hypertension and may precede the increase in blood pressure. We investigated whether transport of the NO precursor L-arginine is related to decreased endothelial function. METHODS AND RESULTS: Radiotracer kinetics ([3H]L-arginine) were used to measure forearm and peripheral blood mononuclear cell arginine uptake in hypertensive subjects (n=12) and in 2 groups of healthy volunteers with (n=15) and without (n=15) a family history of hypertension. In conjunction, forearm blood flow responses to acetylcholine and sodium nitroprusside were measured before and after a supplemental intra-arterial infusion of L-arginine. In vivo and in vitro measures of L-arginine transport were substantially reduced in the essential hypertension and positive family history groups compared with the negative family history group; however, no difference was detected in peripheral blood mononuclear cell mRNA or protein expression levels for the cationic amino acid transporter CAT-1. Plasma concentrations of L-arginine and N(G),N(G')-dimethylarginine (ADMA) did not differ between groups. L-arginine supplementation improved the response to acetylcholine only in subjects with essential hypertension and positive family history. CONCLUSIONS: Similar to their hypertensive counterparts, normotensive individuals at high risk for the development of hypertension are characterized by impaired L-arginine transport, which may represent the link between a defective L-arginine/NO pathway and the onset of essential hypertension. The observed transport defect is not due to apparent alterations in CAT-1 expression or elevated endogenous ADMA.

Acetylcholine↗
PubMed2005

Arterial endothelial function in a porcine model of early stage atherosclerotic vascular disease.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the United States and is projected to become the leading cause of mortality in the world. Atherosclerosis is the most important single factor contributing to this disease burden. In this study, we characterize relationships between endothelial dysfunction and vascular disease in an animal model of diet-induced, early-stage atherosclerotic vascular disease. We tested the hypothesis that hypercholesterolaemia induces vascular disease and impairs endothelium-dependent relaxation (EDR) in conduit arteries of adult male Yucatan pigs. Pigs were fed a normal fat (NF) or high fat cholesterol (HFC) diet for 20-24 weeks. Results indicate that, while the HFC diet did not alter EDR in femoral or brachial arteries, EDR was significantly decreased in both carotid and coronary arteries. Sudanophilic fatty streaks were significantly present in the abdominal aorta and common carotid artery. Histopathology revealed increased intima-media thickness (IMT) and foam cell accumulation in Stary Stage I-III lesions in the abdominal aorta, common carotid artery and femoral arteries. In the coronary arteries, the accumulation of foam cells in Stary Stage I and II lesions resulted in a trend for increased IMT. There was no evidence of vascular disease in the brachial arteries. These results indicate that early stages of CVD (Stary Stage I-III) precede decreases in EDR induced by HFC diet, because femoral arteries exhibited foam cell accumulation and an increased IMT but no change in endothelial function.

Acetylcholine↗
PubMed2003

Protective effect of antioxidants on pulmonary endothelial function after cardiopulmonary bypass.

OBJECTIVES: Pulmonary endothelium-dependent vasodilation is impaired after cardiopulmonary bypass. One explanation might be the generation of reactive oxygen species during the period without flow in the pulmonary artery. The aim of the current study was to investigate if treatment with antioxidants could improve pulmonary endothelial function after cardiopulmonary bypass and influence the blood oxidative status. DESIGN: A prospective, randomized, double-blind study. SETTING: The operating room, intensive care unit, and the biochemistry laboratory in University Hospitals. PARTICIPANTS: Patients scheduled for cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: Treatment with vitamin E, vitamin C, allopurinol, and acetylcysteine (n = 12) or placebo (n = 10). MEASUREMENTS AND MAIN RESULTS: The pulmonary reactivity to an infusion of acetylcholine and markers of oxidative stress in blood were measured before and after cardiopulmonary bypass. Sixteen control patients received saline instead of acetylcholine. Before surgery the pulmonary vascular resistance index decreased during infusion of acetylcholine by 24% and 21% in the treatment and placebo groups. After surgery the decrease was 20% and 8%, respectively, (p = 0.422 and p = 0.026) compared with preoperative response. Pulmonary vasodilation induced by acetylcholine was better maintained in the group treated with antioxidants (p = 0.048). In the treatment group, the blood concentrations of early intermediates of lipid peroxidation were higher, but not that of the end products. Glutathione and oxidized glutathione increased after cardiopulmonary bypass in the treatment group. CONCLUSION: The better maintained endothelium-dependent vasodilation after cardiopulmonary bypass in the treatment group indicated that antioxidant therapy reduced endothelial dysfunction.

Acetylcholine↗
PubMedDate not supplied

Endothelial function and cardiovascular prevention: role of blood lipids, exercise, and other risk factors.

Multifactorial risk factor modification is proven to positively influence morbidity and mortality from both cardiovascular disease and stroke. The vascular endothelium has recently been a focus of interest in cardiovascular prevention. Data suggest that vascular endothelial dysfunction may contribute to the pathophysiology of clinical ischemia, especially angina, myocardial infarction, and sudden death. Endothelial dysfunction includes abnormalities of vasomotor tone (constriction and dilation), balance between fibrinolysis and thrombosis, control of the inflammatory response, and growth of vascular smooth muscle. Cardiovascular prevention interventions have been studied extensively and there are considerable data supporting a beneficial effect on endothelial dysfunction. The interventions that are clearly effective in improving endothelial function are diet and lipid-lowering therapy (especially with statin drugs), use of angiotensin-converting enzyme inhibitors, hormone replacement therapy, vitamin E, and proper physical exercise. Many challenging issues remain unsolved, however, and the endothelium at both the molecular and cellular levels must be further investigated for both research and clinical interests.

Coronary Disease↗
PubMed2005

Endothelial function in pediatric patients on peritoneal dialysis: the need for data.

Cardiovascular complications are emerging as the primary cause of death for patients with childhood end-stage renal disease. Children with end-stage renal failure are subjected to many of the risk factors for cardiovascular disease identified in adult patients. Dysfunction of the endothelium is presently regarded as a first but reversible step in the development of atherosclerosis. Noninvasive techniques to assess endothelial function have been recently developed and have been proven to predict future mortality in adult patients. These techniques are readily applicable to pediatric patients. Endothelial dysfunction has been demonstrated in children in all stages of renal failure. Data on pediatric patients treated with peritoneal dialysis are currently lacking, however. Considering the abundance of cardiovascular risk factors specific to treatment with peritoneal dialysis, such studies should be initiated.

Cardiovascular Diseases↗
PubMed2005

Altered endothelial function in isolated human myometrial vessels induced by plasma from women with pre-eclampsia is not reproducible in isolated mouse vessels.

In order to facilitate characterization of the circulating factor(s) in pre-eclampsia, the present study aimed to determine whether plasma from women with pre-eclampsia, which induces attenuated endothelial-dependent relaxation in human myometrial arteries, is also capable of inducing altered endothelial function in mouse vessels. Human vessels were isolated from myometrial biopsies taken from women with uncomplicated pregnancies (n = 6). Mesenteric and uterine arteries were isolated from male, female, non-pregnant and pregnant C57B mice (n = 24). Vessels were studied using a wire myograph and incubated with plasma (2%) from women with pre-eclampsia (n = 12) or controls (n = 12). Incubation of myometrial vessels from normal pregnant women with plasma from women with pre-eclampsia reduced endothelial-dependent relaxation. This effect was not reproduced in male or female mouse mesenteric or uterine vessels incubated with plasma from women with pre-eclampsia. In conclusion, there are species-specific differences in the actions of the circulating factor(s) on endothelial-dependent relaxation of human and mouse small arteries.

Adult↗
PubMed1992

Improved preservation of endothelial function at 4 degrees C.

Hypothermia combined with chemical cardioplegia is routinely used clinically for perioperative myocardial protection and for donor heart preservation. Profound hypothermia can have an adverse influence on post-preservation endothelial and myocardial functions. In this study, we investigated the effect of temperature on endothelial and myocardial functions following global cardiac ischaemia in the isolated rat heart. A 5-hydroxytryptamine (5-HT)-induced increase in coronary flow was used as a selective probe to assess endothelial function, while myocardial function was measured by a working rat heart model. After recording control observations for endothelial and myocardial functions, hearts were kept ischaemic for 30 or 60 min without cardioplegia (groups 1 and 2, respectively) and for 60, 90 or 120 min following a single infusion of St. Thomas' Hospital solution (groups 3, 4 and 5, respectively). In each group, hearts were kept ischaemic at 20 degrees C or at 4 degrees C (n = 12 in each group). Endothelial and myocardial functions were reevaluated and compared with control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Red wine consumption improves insulin resistance but not endothelial function in type 2 diabetic patients.

Epidemiological studies have shown that red wine consumption is associated with less cardiovascular mortality in the general population and in the diabetic patients. To determine whether red wine improves insulin resistance in diabetic patients and to explore the relation between insulin sensitivity and endothelial function, we studied vascular reactivity and insulin-mediated glucose uptake in 9 type 2 diabetic patients before and after 2 weeks of red wine consumption (360 mL/d, wine-treated diabetics) and 8 type 2 diabetic patients who did not consume wine (control diabetics). Vascular reactivity was evaluated by plethysmography during intraarterial infusion of acetylcholine (Ach), sodium nitroprusside, and L-N-monomethylarginine. Forearm nitrite balance was measured during Ach infusion. Insulin sensitivity was measured by euglycemic hyperinsulinemic clamp at 1 mU/kg per minute. The basal forearm blood flow and the response to Ach, to sodium nitroprusside, and to L-N -monomethylarginine were unchanged both in the wine-treated and in the control diabetics. In contrast, insulin-mediated whole body glucose disposal improved by 43% after red wine consumption (from 2.79 +/- 0.4 to 4.02 +/- 0.5 mg/kg of lean body mass per minute, P = .02), but did not change in the control group. In conclusion, red wine consumption for 2 weeks markedly attenuates insulin-resistance in type 2 diabetic patients, without affecting vascular reactivity and nitric oxide production.

Acetylcholine↗
PubMed2003

[Clinical study on Tianbaokang injection against oxidative injury of vascular endothelial function in ischemic apoplexy].

OBJECTIVE: To discuss clinical effects and therapeutic mechanisms of Tianbaokang Injection on ischemic apoplexy. METHODS: 70 cases of ischemic apoplexy were divided into two groups at random(Tianbaokang group and contrast group, 38 and 32 cases respectively). Clinical effects and indexes of hemorheology and vascular endothelial oxidative injury(SOD activity, MDA content, NO level and ET-1 concentration). RESULTS: The efficiency of Tianbaokang on ischemic apoplexy was 92.1%. Tianbaokang can improve indexes of hemorheology, decrease plasm MDA and ET-1 content, and increase SOD activity and NO level obviously. CONCLUSION: Tianbaokang has better effects on ischemic apoplexy. The therapeutic mechanisms may be related to improving hemorheology, inhibiting lipid peroxidation and vascular endothelial injury, and regulating endothelial function.

Aged↗
PubMed1996

Effect of tetrahydrobiopterin on endothelial function in canine middle cerebral arteries.

Tetrahydrobiopterin is an essential cofactor required for activation of NO synthase. However, in intact arteries, the exact role of tetrahydrobiopterin in the regulation of NO synthase activity is not fully understood. The present study was designed to determine the effect of increasing intracellular tetrahydrobiopterin levels on endothelial function in isolated canine middle cerebral arteries. The arterial segments were incubated in MEM for 24 hours at 37 degrees C in the presence or absence of a tetrahydrobiopterin precursor, sepiapterin (10(-4) mol/L), and/or superoxide dismutase (150 U/mL). The rings were suspended for isometric tension recording. Tetrahydrobiopterin levels were assayed by high-performance liquid chromatography. Production of cGMP was measured by radioimmunoassay. Incubation with sepiapterin markedly increased intracellular tetrahydrobiopterin levels. In sepiapterin-treated arteries, endothelium-dependent relaxations to calcium ionophore A23187 and intracellular cGMP levels were significantly reduced. Superoxide dismutase alone did not affect either relaxation to A23187 or production of cGMP. However, when arteries were incubated with superoxide dismutase plus sepiapterin, endothelium-dependent relaxations to A23187, as well as cGMP production, were significantly augmented. The augmentation of cGMP was observed in rings with (but not without) endothelium. Incubation of arteries in calcium-free medium almost abolished the synergistic effect of tetrahydrobiopterin and superoxide dismutase on cGMP production. These results demonstrate that increased availability of tetrahydrobiopterin may activate endothelial NO synthase. This effect appears to be critically dependent on the presence of superoxide dismutase.

Animals↗
PubMed2000

Tetrahydrobiopterin improves endothelial function in patients with coronary artery disease.

Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase (NOS) and a scavenger of oxygen-derived free radicals. Decreased availability of BH4 leads, under in vitro conditions, to reduced nitric oxide (NO) production and increased superoxide formation. We studied the effect of exogenous BH4 on endothelial function of angiographically normal vessel segments in patients with coronary artery disease. Nineteen patients with coronary artery disease underwent quantitative coronary angiography with simultaneous coronary flow velocity measurements (Cardiometrics FloWire). Data were obtained in angiographically normal segments of the left coronary artery at baseline, after intracoronary (i.c.) administration of acetylcholine (Ach; 10(-4) M), after infusion of BH4 (10(-2) M), and after co-infusion of ACh and BH4. At the end of the study, 300 microg nitroglycerin (NTG) i.c. was administered to obtain maximal vasodilation. At each step, flow velocity was determined before and after 18 microg adenosine i.c. to assess coronary flow velocity reserve. In 15 patients, ACh induced coronary vasoconstriction of -18 +/- 3% (endothelial dysfunction; p < 0.0001 vs. baseline), and in four patients, vasodilation of +39 +/- 20%. In the 15 patients with endothelial dysfunction, BH4 alone did not influence vessel area but prevented vasoconstriction to ACh (+2 +/- 3%, NS, vs. baseline). Correspondingly, calculated volume flow showed the highest value after co-infusion of ACh and BH4. Coronary flow velocity reserve was comparable during the various infusion steps. BH4 prevents ACh-induced vasoconstriction of angiographically normal vessels in patients with coronary artery disease. Thus substitution of this cofactor of NOS may represent a new approach for the treatment of endothelial dysfunction.

Acetylcholine↗
PubMed1994

Hyperlipidaemia does not impair vascular endothelial function in glycogen storage disease type 1a.

Patients with glycogen storage disease type 1 (GSD-1) often have marked hyperlipidaemia with abnormal lipoprotein profiles. This metabolic abnormality improves, but is not fully corrected, with dietary therapy and therefore these patients may be at high risk for the development of atherosclerosis. Endothelial dysfunction is an early event in atherogenesis and can be detected in children and young adults at high risk. We studied endothelial function, using a non-invasive ultrasonographic method, in the brachial arteries of 6 adult GSD-1a patients (aged 23-33 years) with mean cholesterol of 7.9 mmol/l (range 4.7 to 14.6) and mean triglycerides of 9.1 mmol/l (range 4.1 to 21.3), and 12 age- and sex-matched normolipidaemic controls. Flow-mediated (endothelium-dependent) dilation was similar in patients and controls (8.2% vs. 10.5%; P = 0.20). Although the patient numbers are small, these results are consistent with the surprising lack of clinically evident atherosclerosis in GSD-1. The reasons these patients appear less susceptible to the damaging arterial effects of hyperlipidaemia are unknown. These results may have implications for others with secondary hyperlipidaemias.

Adult↗
PubMed2002

Circulating autoantibodies to oxidized LDL correlate with impaired coronary endothelial function after cardiac transplantation.

OBJECTIVE: The oxidative modification of low density lipoprotein (LDL) may play a role in the pathogenesis of transplant-associated arteriosclerosis. Oxidized LDL (OxLDL) is immunogenic as well as atherogenic, and the level of autoantibodies to OxLDL has been taken as an index of the oxidant state of LDL. Because endothelial dysfunction is key in the initiation of transplant-associated arteriosclerosis, we postulated that the level of OxLDL autoantibody is associated with the degree of impairment of coronary endothelial function. METHODS AND RESULTS: Coronary endothelium-dependent dilation was assessed by using intracoronary acetylcholine and endothelium-independent dilation by nitroglycerin in 36 cardiac transplant recipients within 1 year of transplantation. The coronary responses to acetylcholine ranged from -37% (vasoconstriction) to 31% (vasodilation), and the responses to nitroglycerin ranged from 0% to 42% (vasodilation). The coronary vasomotor response to acetylcholine was significantly and inversely related to OxLDL autoantibody levels (r=-0.43, P<0.01) but not LDL levels (r=-0.04, P=0.83) or circulating OxLDL levels detected by monoclonal antibody EO6 (r=-0.27, P=0.11). The coronary artery response to nitroglycerin was not related to levels of OxLDL autoantibodies, LDL, or EO6 (all P=NS). CONCLUSIONS: Autoantibodies to OxLDL are increased in patients with coronary endothelial dysfunction in the first year after cardiac transplantation. The oxidative modification of LDL by inducing endothelial dysfunction in cardiac transplant recipients may be a critical step in the atherogenic effects of LDL and may provide a potential target for therapy.

Acetylcholine↗
PubMed2002

Simvastatin and markers of endothelial function in patients undergoing continuous ambulatory peritoneal dialysis.

Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) are prone to dyslipidemia and have a high risk of cardiovascular death. The aim of this study was to assess the effects of a 6-month treatment with simvastatin (10 mg at bedtime) on markers of endothelial cell injury in 12 hypercholesterolemic CAPD patients. Cholesterol and low-density lipoprotein cholesterol fell significantly after 1 month of therapy. Simvastatin treatment significantly decreased concentrations of vascular cell adhesion molecule and intracellular adhesion molecule after 3 and 6 months of the therapy, respectively. Thrombomodulin decreased significantly after 6 months of the treatment, whereas von Willebrand's factor, P-selectin and E-selectin remained unaltered during simvastatin therapy. Simvastatin, an effective hypolipemic agent, favorably affects endothelial function and may potentially slow the progression of atherosclerosis and confer protection from thrombotic complications in patients with hypercholesterolemia undergoing CAPD.

Biomarkers↗
PubMed2003

Effects of phenolics on vascular endothelial function.

PURPOSE OF REVIEW: There continues to be considerable interest in the concept that antioxidant therapy may reduce cardiovascular risk. Phenols have antioxidant properties and may be important micronutrients. Epidemiological studies have demonstrated a strong link between phenolic intake and reduced cardiovascular risk, but the mechanism of benefit has not been determined. RECENT FINDINGS: Recent evidence has emerged that a number of phenolic compounds, particularly flavonoids, reverse vascular endothelial dysfunction. The normal endothelium plays a critical role in regulating vascular function, and endothelial dysfunction is associated with increased cardiovascular risk. The present article reviews the links between phenolic intake, endothelial function and cardiovascular risk. SUMMARY: Endothelium-derived nitric oxide bioactivity appears to be increased by supplementation with a number of phenols, and this may explain some of the favourable effects of high phenolic intake seen in epidemiological studies.

Animals↗
PubMed1998

Role of NO and angiotensin II in the early development of endothelial functions impairment and cardiac hypertrophy in deoxycorticosterone acetate-salt hypertension.

This study was designed to investigate the effects of chronic inhibition of NO synthesis as well as chronic angiotensin receptor blockade with losartan in the development of hypertension, on mesenteric arterial bed reactivity as well as on the development of cardiac and kidney hypertrophy in deoxycorticosterone-salt (DOCA) hypertension. Uninephrectomized rats were divided in four experimental groups all receiving saline water to drink and treated or not with losartan over a period of 9 days. Two of these groups were administered DOCA, one of which received also N(G)-nitro-L-arginine-methyl ester (L-NAME) to drink. A third group received only L-NAME, while another group received only saline. Systolic blood pressure was similarly increased in L-NAME, DOCA, DOCA-L-NAME groups. Cardiac and kidney weights were increased in DOCA but significantly reduced in DOCA-L-NAME. Losartan prevented the development of hypertension in all groups and also prevented cardiac and kidney hypertrophy in DOCA. The hyperreactivity of mesenteric arteries to phenylephrine, measured in the presence of indomethacin, was endothelium-dependent in both L-NAME groups but not in DOCA rats. Pretreatment with BQ 123 did not modify these endothelium-dependent responses in L-NAME rats. Chronic losartan prevented endothelium-dependent phenylephrine hyperreactivity only in DOCA, whereas only the removal of the endothelium attenuated the responsiveness in both L-NAME-treated groups. Vasorelaxations to acetylcholine and isoproterenol were attenuated in the three hypertensive groups and were normalized only in DOCA and L-NAME treated with losartan. In summary, in all hypertensive groups, blood pressure was normalized by losartan independently of its effects on endothelial functions. In DOCA, losartan normalized the phenylephrine hyperreactivity through an endothelial-dependent mechanism. However, in L-NAME-treated groups an endothelial-derived contracting factor, other than angiotensin II, endothelin, or vasoconstrictor prostanoids, appears to be activated. Both NO and angiotensin II seem to play a role in the early development of hypertension and organ hypertrophy in DOCA hypertension.

Angiotensin II↗
PubMed2001

Risk factors of atherosclerosis and saphenous vein endothelial function.

BACKGROUND: Impaired vasomotor function has been suggested as playing a role in the pathophysiology of atherosclerosis and it may also affect the late patency of bypass grafts. We evaluated, in vitro, the influence of risk factors of atherosclerosis on saphenous vein endothelial function in patients with cardiovascular diseases. METHODS: Forty-five saphenous vein rings with intact (E+) and denuded endothelium (E-) were studied. The following drugs were used: norepinephrine (NE), acetylcholine (Ach), histamine (H) and serotonine (5-HT). RESULTS: Contraction to norepinephrine (n=15) showed a maximal tension of 783+/-115 percent that was increased in diabetics, smokers, and patients with hypertension. There was a wide range of response to acetylcholine in rings with intact endothelium (n=25), (mean relaxation 16.4+/-1.7 percent, ranging from -22.2 percent to 45 percent) with relaxation (26+/-1.1 percent) and contraction (-11+/-1.2 percent); relaxation was reduced in patients with hypertension and in diabetics (7.4+/-2.6 percent vs non diabetics 24.4+/-1.73 percent; p<0.01). Five of the 12 veins from diabetics exibited contraction (10+/-1.48 percent). Histamine (n=15) caused moderate relaxation at low doses (25+/-2.46 percent) followed by contraction at higher concentrations (184+/-5.7 percent). This was greater in diabetics (193+/-6.8 percent vs non diabetics 157+/-5.3 percent; p=0.045) while in preparations without endothelium (n=10) only relaxation was obtained (45+/-2.89 percent). Contraction (242+/-7.4 percent) was observed in response to serotonine (n=15) that was not affected by endothelial removal. In this study saphenous vein: (1) exhibited a wide range of responses to acetylcholine; (2) evoked marked contraction to norepinephrine and serotonine; (3) elicited contraction in response to histamine that was endothelium-dependent, suggesting the production or the release of an endothelium-derived-contracting-factor (EDCF). CONCLUSIONS: Saphenous vein is able to secrete a contracting factor in patients with risk factors of atherosclerosis and above all diabetes. The mechanisms that regulate the balance between the relaxing and contracting factors and how the endothelial cells become the source of the substances with vasoconstrictor activity remain to be determined.

Acetylcholine↗