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Results for “Endothelial function”

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At least 325 records · Page 18Linked to original sources

PubMed2002

Long-term improvement in homocysteine levels and arterial endothelial function after 1-year folic acid supplementation.

PURPOSE: Hyperhomocysteinemia, a risk factor for atherosclerosis, is associated with endothelial dysfunction that can be improved with short-term folic acid supplementation. The current study aimed to assess whether folic acid supplementation could produce longer-term improvements in homocysteine levels and arterial endothelial function. SUBJECTS AND METHODS: Twenty-nine healthy adults with hyperhomocysteinemia were selected from 89 volunteers enrolled in a community-based atherosclerosis screening project. All subjects were given folic acid (10 mg/d) for 1 year. Fasting plasma homocysteine levels were measured by high-performance liquid chromatography. Arterial endothelial function was measured as flow-mediated dilation of the brachial artery using high-resolution B-mode ultrasound. RESULTS: Folic acid supplementation for 1 year was associated with a significant increase in mean (+/-SD) plasma folate levels (24 +/- 5 nmol/L to 40 +/- 5 nmol/L; P < 0.001) and a significant decline in homocysteine levels (9.0 +/- 1.7 micromol/L to 7.9 +/- 2.0 micromol/L; P < 0.001). Flow-mediated dilation also improved significantly, from 7.4% +/- 2.0% to 8.9% +/- 1.5% (P <0.0001), but there was no change in nitroglycerin-induced (endothelium-independent) responses. CONCLUSIONS: These results demonstrate that long-term folic acid improves arterial endothelial function and has potential implications for the prevention of atherosclerosis in adults with hyperhomocysteinemia.

Adult↗

PubMed2005

[Change of endothelial function with aging].

Vascular endothelium plays important roles in vascular relaxing, anti-atherosclerotic, or anti-thrombotic effect through production of vasoactive substances such as nitric oxide. Accumulated evidences suggest that endothelial dysfunction is the initial step in the development of atherosclerosis. Recently, less invasive or non-invasive method such as venous occlusion plethysmography and measurement of flow-mediated dilatation has been developed to evaluate endothelial function. Several investigations using these methods showed that endothelial function is impaired with aging. The mechanism of endothelial dysfunction with aging remains to be fully elucidated, although oxidative stress may be involved in impairment of endothelial function.

Aged↗

PubMed2003

Troglitazone therapy improves endothelial function to near normal levels in women with polycystic ovary syndrome.

Obese women with polycystic ovary syndrome (PCOS) exhibit impaired endothelial function, which is strongly and directly correlated with both testosterone levels and insulin resistance. Endothelial dysfunction is considered a potent risk factor for macrovascular disease. Because troglitazone (Tgz) improves both hormonal profiles and insulin sensitivity, we tested whether Tgz treatment ameliorates endothelial function in these patients. We studied leg blood flow (LBF) responses to graded intrafemoral artery infusion of the endothelium-dependent vasodilator methacholine chloride (MCh) and to a 4-h hyperinsulinemic euglycemic clamp (120 mU/m(2) x min) in 10 PCOS, before and after 3 months treatment with Tgz (600 mg/d). A group of 13 obese women (OBW) matched for age, weight, body fat (>40% in both groups), blood pressure, and total cholesterol served as controls. PCOS patients exhibited elevated free testosterone (fT) and triglycerides (TG) and lower high density lipoprotein cholesterol levels compared with OBW [14.0 +/- 1.0 vs. 3.7 +/- 0.6 pmol/liter (P < 0.0001), 1.60 +/- 0.28 vs. 0.94 +/- 0.09 mmol/liter (P < 0.02), and 0.91 +/- 0.04 vs. 1.1 +/- 0.04 mmol/liter (P < 0.005), respectively]. Tgz treatment reduced fT levels, but did not improve the TG and high density lipoprotein profile [to 9.7 +/- 2.8 pmol/liter (P < 0.007), 1.49 +/- 0.34 mmol/liter (P = NS), and 0.93 +/- 0.07 mmol/liter (P = NS), respectively]. Basal LBF was unchanged after Tgz. In PCOS compared with OBW, insulin stimulated glucose disposal (52.7 +/- 6.6 vs. 85.5 +/- 4.4 micromol/kg fat-free mass x min; P < 0.0005) and vasodilation (increase in LBF, 22 +/- 14% vs. 59 +/- 15%; P < 0.05) were significantly improved after Tgz treatment to 68.8 +/- 7.2 micromol/kg fat-free mass x min (P < 0.0001) and 101 +/- 48% (P < 0.03), respectively. The increase in LBF in response to MCh in PCOS was markedly more pronounced after treatment (P < 0.01, by ANOVA) and was similar to that observed in OBW. Before Tgz treatment, maximal LBF increments in response to MCh were 130 +/- 25% and 233 +/- 29% in PCOS and OBW, respectively (P < 0.01). After Tgz treatment, PCOS values improved, achieving increments similar to those in OBW (245 +/- 45%; P < 0.04). Tgz treatment in PCOS improves both hormonal and metabolic features. These modifications are associated with improvement of endothelial function, suggesting that Tgz could be a useful tool to reduce the risk of macrovascular disease in women with PCOS and perhaps in other insulin-resistant syndromes.

Blood Glucose↗

PubMed2001

Vascular endothelial function in cyclosporine and tacrolimus treated renal transplant recipients.

BACKGROUND: Endothelial dysfunction is an early key event in the development of arteriosclerotic cardiovascular disease (ASCVD), thus an early marker of subclinical ASCVD. Endothelial function is impaired in renal transplant recipients (RTR) treated with cyclosporine (CyA). Tacrolimus is associated with less hyperlipidemia and hypertension than CyA, however, there are no data on endothelial function in tacrolimus-treated RTR. METHODS: High-resolution brachial ultrasonography was used to assess endothelium-dependent dilatation (EDD), and endothelium-independent dilatation (EID) in 20 stable RTR and a control group of 10 healthy subjects without clinical evidence of ASCVD. The RTR group included patients receiving CyA (n=10) and tacrolimus (n=10). EDD and EID were measured as percent increase in brachial artery diameter in response to reactive hyperemia and nitroglycerin, respectively. RESULTS AND CONCLUSIONS: EDD was significantly lower in RTR versus controls (1.7+/-0.7 vs. 7.3+/-0.7%, P<0.0001), whereas EID was similar in the two groups. No significant differences were found in EDD or in EID between CyA- and tacrolimus-treated RTR. Glomerular filtration rate, plasma homocysteine, blood pressure, and lipid profiles were similar in CyA- and tacrolimus-treated RTR.

Adult↗

PubMed2006

Role of endothelial function and inflammation in patients with cardiovascular risk factors, with and without a history of myocardial infarction.

BACKGROUND: Endothelial dysfunction and inflammation, in particular their lack of improvement after risk reduction, might better reflect advanced atherosclerosis than just the presence of risk factors. The aim of this study was to compare endothelial function and inflammatory parameters in high-risk patients who had no history of myocardial infarction and in patients in a stable phase after myocardial infarction. METHODS: We compared endothelial function of the brachial artery, measured using high-resolution ultrasound, in 45 patients with hyperlipidaemia (Group 1), and in 45 patients in a stable period after myocardial infarction (Group 2). Forty-five healthy individuals served as a control group (Group 3). RESULTS: Compared to patients with treated hyperlipidaemia, patients after myocardial infarction had lower values of total and LDL cholesterol (p = 0.015; 0.005) and homocysteine (p < 0.005), but marginally higher IL-6 levels (p = 0.1). Other measurements were comparable. However, flow-mediated dilation of the brachial artery was significantly diminished in patients after myocardial infarction (10.6 +/- 3.0; 5.9 +/- 4.0; 14.0 +/- 1.9% for Groups 1-3; ANOVA p = 0.0001; respectively). CONCLUSIONS: We found that patients with previous myocardial infarction have substantially lower endothelial function and increased some inflammatory parameters than patients with a similar level of atherosclerotic risk profile but without clinically evident coronary artery disease.

Adult↗

PubMed2006

Simvastatin treatment improves endothelial function and increases fibrinolysis in patients with hypercholestrolemia.

OBJECTIVES: Statins reduce cardiovascular events by cholesterol-lowering as well as nonlipid-related actions. Thrombin activatable fibrinolysis inhibitor (TAFI) is a recently identified independent risk factor of thrombosis. Endothelial dysfunction is also a strong predictor of cardiovascular events. The aim of this study was to assess the effects of simvastatin treatment on circulating TAFI concentrations and endothelial function in patients with hypercholesterolemia. METHODS: Thirty-five patients (19 female, mean age 48 +/- 7 years) with hyperlipidemia were recruited into the study. Simvastatin was administered, 40 mg daily, for eight weeks to all subjects. Study subjects did not receive any medication except for lipid-lowering therapy during the follow-up period. Endothelial function was evaluated by flow-mediated dilation (FMD) from the brachial artery of the patients. Plasma lipid parameters, TAFI levels and endothelial function were measured before and after simvastatin treatment. RESULTS: Treatment with simvastatin showed a significant decrement in plasma total cholesterol, LDL cholesterol and triglyceride levels (p<0.05). Plasma TAFI levels were also significantly decreased after simvastatin treatment [median 17.0 (range 0.4-93.7) mcg/mL versus median 6.9 (range 0.8-63.0) mcg/mL, p<0.001]. Mean FMD was measured 7.7 +/- 2.5% at baseline and significantly improved after treatment (13.0 +/- 1.4%) (p=0.001). CONCLUSION: Our findings of decreased TAFI levels may reflect the beneficial effect of simvastatin treatment on fibrinolysis, and improved endothelial function may suggest the improved future cardiovascular events in hyperlipidemic patients.

Anticholesteremic Agents↗

PubMed2007

Acute effects of hyperglycaemia with and without exercise on endothelial function in healthy young men.

Post-prandial hyperglycaemia impairs endothelial function as evaluated by brachial artery flow-mediated dilation (FMD). Exercise is an intervention to protect against cardiovascular disease and to improve FMD. In this study, we examined whether the effect of acute hyperglycaemia on endothelial function in healthy young men is restored by aerobic exercise. Using a counterbalanced, randomized crossover design, we measured the brachial artery FMD at baseline and 1, 2, 3 and 4 h after 75 g glucose ingestion in 11 healthy young men, with and without a single bout of aerobic exercise. Brachial artery FMD declined from 11.4 +/- 3.8% at baseline to 7.3 +/- 3.4% 1 h after oral glucose ingestion, and returned to baseline after 4 h. When the oral glucose ingestion was followed immediately by 45 min of treadmill exercise at an intensity of 60% maximal oxygen uptake, FMD demonstrated no significant decrease (11.8 +/- 2.5, 11.3 +/- 2.8, 12.2 +/- 2.7, 13.5 +/- 3.5, and 12.6 +/- 2.4% at baseline and 4 h after ingestion, respectively). The results indicate that the aerobic exercise restores the impaired FMD induced by oral glucose ingestion.

Adult↗

PubMed2004

Effect of passive smoking on endothelial function in: healthy adults.

BACKGROUND: Active smoking predisposes to atherosclerotic vascular disease but recent evidence that inhalation of environmental tobacco smoke (passive smoking) may also have deleterious cardiovascular effects, has enormous public health implications. Endothelial dysfunction is an important early feature of atherogenic process, which may occur due to passive smoking. OBJECTIVE: To assess the effect of passive smoking on endothelial function (measured by flow-mediated dilatation, a marker of endothelium-dependent arterial dilatation) and compare it with non-smokers. STUDY DESIGN: Case control study. SETTING: Out-Patient Department of Medicine, Government Medical College, Nagpur. PARTICIPANTS: Seventy-five young, healthy, male adults between 15-30 years age were studied. There were three groups: (a) Non smokers (n = 25) (b) Passive smokers (n= 25) and (c) Active smokers (n = 25). Subjects with diabetes mellitus, hypertension and ischemic heart disease were excluded. Lipid profile was measured in all. Endothelial function was tested non-invasively by using high frequency linear vascular probe on brachial artery. Resting brachial artery lumen, flow at rest and after hyperemia, flow-mediated dilatation and nitroglycerine-induced dilatation were measured. RESULTS: The mean brachial artery lumen dilatation and flow at rest were similar in all the three groups. Flow-mediated dilatation (FMD%, a marker of endothelium-dependent dilatation and endothelial function) was significantly higher in non-smokers than passive smokers (8.9 +/- 4.8 Vs 5 +/- 2.3, p < 0.01) and also as compared with active smokers (8.9 +/- 4.8 Vs 6.6 +/- 2.2, p < 0.05). Nitroglycerine-induced dilatation, (a marker of endothelium-independent dilatation ) was similar in all the three groups. Serum lipids (mean cholesterol, LDL, and mean LDL/HDL ratio) were statistically significantly higher in passive and active smokers as compared with non-smokers (p < 0.05). CONCLUSION: Like active smoking, passive smoking was also associated with impaired endothelial function, (a key early event in atherogenesis) and altered lipid profile, in healthy young adults.

Adolescent↗

PubMed1995

Effects of vitamin E on endothelial function in men after myocardial infarction.

This study showed that endothelial dysfunction is present in men 3 to 6 months after myocardial infarction, but was unable to show any improvement in endothelial function after 3 months of therapy with vitamin E 800 IU/day. Further studies are necessary to determine whether higher doses or a longer course of vitamin E, or whether other antioxidant agents with or without lipid-modifying activity, would improve endothelial function.

Acetylcholine↗

PubMed2006

Chronic antioxidant supplementation impairs coronary endothelial function and myocardial perfusion in normal pigs.

Experimental studies have shown the beneficial effects of antioxidant supplementation on endothelial function in the presence of increased endogenous oxidative stress, whereas limited data are available under normal conditions. The present study tested the hypothesis that in normal pigs long-term antioxidants would have deleterious effects on the cardiovascular system. Normal domestic pigs (V, n=6) were studied 12 weeks after dietary supplementation with vitamin E (100 IU/kg per day) and vitamin C (1 g/day) and compared with normal controls (C, n=7). Myocardial perfusion and permeability index were evaluated by electron beam computed tomography after intravenous adenosine and dobutamine. Coronary endothelial function was evaluated in vitro by organ chamber and coronary tissue studied by immunoblotting and staining. Myocardial perfusion response was lower in V than in C after adenosine (10.1+/-4.5 versus 53.4+/-5.2%; P<0.01) and dobutamine (V, 78.4+/-8.1; C, 193.0+/-39.0%; P<0.05). The permeability index increased in V after adenosine (48.8+/-5.1%) and dobutamine (59.9+/-13.6%) and did not change in C. Coronary vasodilation to bradykinin and substance P was lower in V than in C. Moreover, in V, coronary nitrotyrosine and superoxide content was significantly higher than in C. The groups had similar total monomer expression of endothelial nitric oxide synthase, whereas the dimerized form, reflecting coupled enzyme, was lower in V. These findings suggest that long-term experimental antioxidant vitamin supplementation in normal pigs impairs myocardial perfusion and coronary endothelial function via an increased level of oxidative stress in the arterial wall, which may be partly related to the uncoupling of endothelial nitric oxide synthase and/or the direct prooxidant effect of vitamin radicals.

Animals↗

PubMed2006

Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols.

Endothelial dysfunction is an early pathophysiological feature and independent predictor of poor prognosis in most forms of cardiovascular diseases. Epidemiological studies report an inverse association between dietary flavonoid consumption and mortality from cardiovascular diseases. In the present paper, we review the effects of flavonoids, especially quercetin and wine polyphenols, on endothelial function and dysfunction and its potential protective role in hypertension, ischemic heart disease and stroke. In vitro studies show that flavonoids may exert multiple actions on the NO-guanylyl cyclase pathway, endothelium-derived hyperpolarizing factor(s) and endothelin-1 and protect endothelial cells against apoptosis. In vivo, flavonoids prevent endothelial dysfunction and reduce blood pressure, oxidative stress and end-organ damage in hypertensive animals. Moreover, some clinical studies have shown that flavonoid-rich foods can improve endothelial function in patients with hypertension and ischemic heart disease. Altogether, the available evidence indicates that quercetin and wine polyphenols might be of therapeutic benefit in cardiovascular diseases even though prospective controlled clinical studies are still lacking.

Cardiovascular Diseases↗

PubMed1997

Improvement in endothelial function by angiotensin converting enzyme inhibition in insulin-dependent diabetes mellitus.

We postulated that nitric oxide (NO)-mediated endothelial function would be improved by acute and short-term treatment with an angiotensin converting enzyme (ACE) inhibitor in patients with type I diabetes mellitus, in whom endothelial function is depressed. Nine type I diabetic patients and eight healthy subjects underwent forearm blood flow measurement using strain gauge plethysmography during intraarterial infusion of incremental doses of endothelium-dependent (acetylcholine [ACh]) and endothelium-independent (sodium nitroprusside [SNP]) vasodilators. Pretreatment ACh responses were depressed in diabetic patients relative to the normal subjects (P < 0.05). No difference between the groups was evident in response to SNP. Acute ACE inhibition (with intrabrachial enalaprilat) enhanced ACh responses in the diabetic patients (P < 0.005), with a further improvement evident after 1 mo of oral therapy with enalapril (P < 0.001) when ACh responses were normalized. ACE inhibition did not affect SNP responses. We conclude that acute administration of the ACE inhibitor, enalaprilat, enhances NO-mediated endothelial function in type I diabetic patients, with further improvement evident after 4 wk of enalapril therapy.

Administration, Oral↗

PubMed2003

Assessment of peripheral vascular endothelial function with finger arterial pulse wave amplitude.

BACKGROUND: Abnormalities in pulse wave amplitude (PWA) have been described in subjects with atherosclerosis and may be a marker of future cardiac events. We evaluated the relationship between changes in PWA of the finger and peripheral endothelial function. METHODS: We performed measurements of PWA with a novel finger plethysmograph (peripheral arterial tonometry [PAT]) and compared the findings with a simultaneous noninvasive measurement of peripheral endothelial function with brachial artery ultrasound scanning (BAUS) in 89 subjects. The PAT hyperemia ratio was defined as the ratio of PWA during reactive hyperemia relative to the baseline. Flow-mediated dilation (FMD) was defined by BAUS as the ratio of the brachial artery diameter during reactive hyperemia relative to the baseline. Sixty-eight subjects underwent exercise myocardial perfusion imaging (ExMPI). RESULTS: Fifty-four men and 35 women were examined. There was a linear relationship between the PAT hyperemia ratio and FMD during the same episode of reactive hyperemia (r = 0.55, P <.0001). Subjects in the lowest FMD quartile had the lowest PAT hyperemia ratio, whereas subjects in the highest FMD quartile had the highest PAT hyperemia ratio (P <.001 for trend). Similar to BAUS, the PAT hyperemia ratio was more impaired in subjects with cardiovascular risk factors and in subjects with ExMPI studies that were indicative of coronary artery disease. CONCLUSIONS: Assessment of PWA with PAT demonstrates patterns of abnormality similar to that of BAUS assessment of FMD. PWA during reactive hyperemia is influenced by factors known to affect endothelial function, including cardiovascular risk factors and coronary artery disease. These findings support the concept that analysis of PWA with PAT during reactive hyperemia may be used to study peripheral vascular endothelial function.

Blood Pressure↗

PubMed2001

Lisinopril improves endothelial function in chronic cigarette smokers.

Cigarette smoking is a pernicious risk factor for the pathogenesis of coronary artery disease, and endothelial dysfunction is an important antecedent event in this process. This is important, as cigarette smoke is directly toxic to endothelial cells. Inhibitors of angiotensin-converting enzyme (ACE) have been shown to improve endothelial function in diabetes and hypercholesterolaemia, and are a promising option in smokers. We treated 23 subjects (age 38+/-12 years; mean+/-S.D.) for 8 weeks with 20 mg of lisinopril in a randomized controlled trial. Endothelial function was assessed by measurement of forearm blood flow responses to intra-arterial infusions of endothelial-dependent and -independent vasodilators and an endothelial-dependent vasoconstrictor [acetylcholine, sodium nitroprusside and monomethyl-L-arginine (L-NMMA) respectively] using venous occlusion plethysmography. Lisinopril significantly increased the forearm blood flow response to acetylcholine by 20% [lisinopril, 3.12+/-0.37 (mean+/-S.E.M.); placebo, 2.58+/-0.25; P=0.02, 95% confidence intervals (CI) 0.09, 1.06] (values given are ratios of flow in the infused arm to that in the control arm); there was no effect on the response to sodium nitroprusside (lisinopril, 3.97+/-0.40; placebo, 3.92+/-0.39; P=0.84; 95% CI -0.50, 0.61). The vasoconstrictor response to L-NMMA demonstrated a significant improvement (lisinopril, 0.77+/-0.06; placebo, 0.95+/-0.05; P<0.001; 95% CI -0.09, -0.27). In conclusion, these results indicate that ACE inhibition can improve endothelial function in cigarette smokers. We show that lisinopril improves both receptor-mediated and tonic NO release. The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release.

Acetylcholine↗

PubMed2004

Repeatability of noninvasive surrogates of endothelial function.

We compared the repeatability of 2 ultrasonographic methods for endothelial function assessment at brachial artery-flow-mediated dilation (FMD) and post-ischemic peak blood flow (PBF). Twenty healthy volunteers were examined twice within 10 days; coefficients of variation were 13.8% for PBF and 41.0% for FMD. PBF seems to be superior to FMD in terms of reproducibility. Consequently, smaller noninvasive studies of endothelial function can be designed utilizing PBF compared with FMD.

Adult↗

PubMed2003

Wine and endothelial function.

In recent years many studies have focused on the well-known relationship between wine consumption and cardiovascular risk. Wine exerts its protective effects through various changes in lipoprotein profile, coagulation and fibrinolytic cascades, platelet aggregation, oxidative mechanisms and endothelial function. The last has earned more attention for its implications in atherogenesis. Endothelium regulates vascular tone by a delicate balancing among vasorelaxing (nitric oxide [NO]) and vasoconstrincting (endothelins) factors produced by endothelium in response to various stimuli. In rat models, wine and other grape derivatives exerted an endothelium-dependent vasorelaxing capacity especially associated with the NO-stimulating activity of their polyphenol components. In experimental conditions, reservatrol (a stilbene polyphenol) protected hearts and kidneys from ischemia-reperfusion injury through antioxidant activity and upregulation of NO production. Wine polyphenols are also able to induce the expression of genes involved in the NO pathway within the arterial wall. The effects of wine on endothelial function in humans are not yet clearly understood. A favorable action of red wine or dealcoholized wine extract or purple grape juice on endothelial function has been observed by several authors, but discrimination between ethanol and polyphenol effects is controversial. It is, however likely that regular and prolonged moderate wine drinking positively affects endothelial function. The beneficial effects of wine on cardiovascular health are greater if wine is associated with a healthy diet. The most recent nutritional and epidemiologic studies show that the ideal diet closely resembles the Mediterranean diet.

Animals↗

PubMed1999

The thiazolidinedione rosiglitazone (BRL-49653) lowers blood pressure and protects against impairment of endothelial function in Zucker fatty rats.

Human obesity is associated with insulin resistance, hyperinsulinemia, and a predisposition to hypertension and vascular disease, the origin of which may lie in impairment of endothelial function. We tested the effects of the thiazolidinedione rosiglitazone on blood pressure and endothelial function in insulin-resistant fatty Zucker rats, which display hypertension and abnormal endothelial cell function. We studied fatty Zucker rats given rosiglitazone maleate (50 micromol/kg diet; n = 8) for 9-12 weeks (treated fatty), untreated fatty rats (n = 8), and lean rats (n = 8) given diet alone. At the end of the study, systolic blood pressure was significantly higher in untreated fatty (147 +/- 5 mmHg) than in lean rats (125 +/- 2 mmHg; P < 0.05), but rosiglitazone treatment prevented the development of hypertension in fatty rats (123 +/- 1 mmHg). Fasting hyperinsulinemia in untreated fatty rats (28.7 +/- 6.0 ng/ml) was significantly lowered by rosiglitazone (7.0 +/- 1.4 ng/ml; P < 0.05 vs. untreated fatty), but remained significantly higher than the levels seen in lean rats (1.5 +/- 0.4 ng/ml; P < 0.01). Mesenteric arteries were studied in a myograph. Maximal acetylcholine chloride (1.1 micromol/l)-induced relaxation of norepinephrine hydrochloride (NE)-induced constriction was impaired in untreated fatty (62.4 +/- 3.4%) vs. lean (74.3 +/- 3.5%; P = 0.01) rats; this defect was partially prevented by rosiglitazone (66.5 +/- 3.0%; P = 0.01 vs. untreated fatty). Insulin (50 mU/l) significantly attenuated the contractile response to NE in lean rats (14.7 +/- 3.3%; P = 0.02); this vasodilator effect of insulin was absent in untreated fatty rats at concentrations of 50-5,000 mU/l, but was partially restored by rosiglitazone (9.7 +/- 2.5% attenuation; P = 0.02 vs. no insulin). Thus, rosiglitazone prevents the development of hypertension and partially protects against impaired endothelial function associated with insulin resistance. These latter effects may contribute to the drug's antihypertensive properties.

Acetylcholine↗

PubMed2003

Improvement of serum oxidation by pravastatin might be one of the mechanisms by which endothelial function in dilated coronary artery segments is ameliorated.

BACKGROUND: Oxidation susceptibility of lipids in vitro is considered to reflect the exposure of lipids to oxidation stress in vivo which is related to cardiovascular morbidity. This study examined the effect of pravastatin therapy on serum oxidation susceptibility, particularly in relation to endothelial function of coronary arteries. METHODS: The participants were recruited from the Pravastatin-Related Effects Following Angioplasty on Coronary Endothelium trial, a double-blinded, placebo-controlled, randomized, multi-center study designed to analyze the effect of pravastatin treatment on endothelial function in previously dilated and normal coronary arteries. Serial, graded, intra-coronary acetylcholine infusions were used to assess endothelial function. In vitro, copper-induced, serum oxidation parameters were determined at randomization and at time of coronary endothelial function assessment. RESULTS: Oxidation parameters were determined in 45 patients (pravastatin 23, placebo 22). Pravastatin therapy significantly improved serum oxidation lag time (+8%, P<0.05), maximal diene formation rate (-22%, P<0.01) and total amount of dienes formed after 5 h (-16%, P<0.01). These parameters remained essentially unchanged in the placebo group. Acetylcholine-evoked responses were positively correlated to therapy-induced change in serum oxidation susceptibility in the dilated segment group (r2=0.56, P=0.006). CONCLUSION: Pravastatin's beneficial effect on endothelial dysfunction of dilated coronary segments may be secondary to pravastatin's improvement of oxidation susceptibility.

Acetylcholine↗