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Results for “Endothelial function”

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PubMed2002

Reduction of inflammatory cytokine concentrations and improvement of endothelial functions in obese women after weight loss over one year.

BACKGROUND: Visceral fat is a key regulator site for the process of inflammation, and atherosclerotic lesions are essentially an inflammatory response. METHODS AND RESULTS: Fifty-six healthy premenopausal obese women (age range 25 to 44 years, body mass index 37.2+/-2.2, waist to hip ratio range 0.78 to 0.92) and 40 age-matched normal weight women were studied. Compared with nonobese women, obese women had increased basal concentrations of tumor necrosis factor-alpha (TNF-alpha, P<0.01), interleukin-6 (IL-6, P<0.01), P-selectin (P<0.01), intercellular adhesion molecule-1 (ICAM-1, P<0.02), and vascular adhesion molecule-1 (VCAM-1, P<0.05). Vascular responses to L-arginine (3 g IV), the natural precursor of nitric oxide, were impaired in obese women: reductions in mean blood pressure (P<0.02), platelet aggregation to adenosine diphosphate (P<0.05), and blood viscosity (P<0.05) were significantly lower as compared with those in the nonobese group. Concentrations of TNF-alpha and IL-6 were related (P<0.01) to visceral obesity, as well as to adhesin levels and responses to L-arginine. After 1 year of a multidisciplinary program of weight reduction (diet, exercise, behavioral counseling), all obese women lost at least 10% of their original weight (9.8+/-1.5 kg, range 7.5 to 13 kg). Compared with baseline, sustained weight loss was associated with reduction of cytokine (P<0.01) and adhesin (P<0.02) concentrations and with improvement of vascular responses to L-arginine. CONCLUSION: In obese women, endothelial activation correlates with visceral body fat, possibly through inappropriate secretion of cytokines. Weight loss represents a safe method for downregulating the inflammatory state and ameliorating endothelial dysfunction in obese women.

Adult↗

PubMed2006

Chlorogenic acid attenuates hypertension and improves endothelial function in spontaneously hypertensive rats.

BACKGROUND AND OBJECTIVES: Epidemiologic studies indicate that ingestion of vegetables and fruit inhibits the development of cardiovascular disease. Chlorogenic acids are abundant phenolic compounds contained in vegetables and fruits, but the impact of dietary chlorogenic acids on vascular function in hypertension is not known. We therefore examined the effects of 5-caffeoylquinic acid (CQA), a representative chlorogenic acid, on blood pressure and vascular function in age-matched normotensive Wistar-Kyoto rats and spontaneously hypertensive rats. METHODS AND RESULTS: A single ingestion of CQA (30-600 mg/kg) reduced blood pressure in spontaneously hypertensive rats, an effect that was blocked by administration of a nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester. When spontaneously hypertensive rats were fed diets containing 0.5% CQA for 8 weeks (approximately 300 mg/kg per day), the development of hypertension was inhibited compared with the control diet group. CQA ingestion increased urinary excretion of nitric oxide metabolites and decreased urinary excretion of hydrogen peroxide; decreased NADPH-dependent superoxide anion production in the aorta, suggesting that dietary CQA inhibited vascular NADPH oxidase activity; significantly improved acetylcholine-induced endothelium-dependent vasodilation in the aorta; and markedly reduced the degree of immunohistochemical staining for nitrotyrosine and media hypertrophy in aorta sections. In contrast, CQA had no effects in Wistar-Kyoto rats. CONCLUSIONS: Dietary CQA reduces oxidative stress and improves nitric oxide bioavailability by inhibiting excessive production of reactive oxygen species in the vasculature, and leads to the attenuation of endothelial dysfunction, vascular hypertrophy, and hypertension in spontaneously hypertensive rats.

Animals↗

PubMed1991

Endothelial function in human coronary arteries in vivo. Focus on hypercholesterolemia.

To examine whether and to what extent hypercholesterolemia may affect the vasoactive role of the endothelium before the onset of angiographically visible atherosclerosis in the coronary circulation, we studied normal subjects (group 1, n = 11), individuals with elevated low density lipoprotein plasma values but angiographically smooth coronary arteries (group 2, n = 8), and patients with hypercholesterolemia and minimal disease of the vessel under study (group 3, n = 8). Coronary vasomotor function was evaluated by three interventions: subselective intracoronary infusion of acetylcholine (0.036, 0.36, and 3.6 micrograms/min) with a 3F Doppler catheter in the left anterior descending artery, 0.3 mg intracoronary nitroglycerin ("endothelium-independent"), and increase in blood flow (assessment of flow-dependent, endothelium-mediated coronary dilation). In group 1, all interventions caused coronary dilation of the left anterior descending artery as assessed by automatic quantification of digitized cineframes. However, in group 2, acetylcholine elicited substantial coronary vasoconstriction, and the vasodilator response to nitroglycerin and to increases in flow (flow-dependent dilation) was preserved. In group 3, the acetylcholine-induced coronary vasoconstriction was even more pronounced, and the flow-dependent dilation was impaired (+5.1 +/- 1% versus +10.5 +/- 1.1% [group 1], p less than 0.05). The coronary flow reserve (derived from Doppler flow velocity measurements) in response to papaverine was not significantly different in normal and hypercholesterolemic individuals (groups 2 and 3). However, the increase in coronary flow exerted by acetylcholine was substantially depressed in patients with hypercholesterolemia (groups 2 and 3) as compared with normal individuals (+48 +/- 8.3% and +49 +/- 25% versus +220 +/- 28.5%, respectively, p less than 0.01). Thus, hypercholesterolemia elicits endothelial dysfunction in coronary conduit and resistance vessels in humans that precedes angiographically visible atherosclerotic lesions in large coronary arteries. Conceivably, these vascular alterations contribute to increased coronary vasomotor tone within the coronary circulation and may predispose these patients to myocardial ischemia.

Acetylcholine↗

PubMed1998

Mechanisms of Impaired Endothelial Function Associated With Insulin Resistance.

BACKGROUND: The insulin-resistant (IR) syndrome is causally related to hypertension and cardiovascular events; however, the underlying mechanism remains elusive. The current study was designed to determine (1) whether the IR syndrome causes vascular dysfunction and (2) whether insulin resistance alters the activity of the individual endothelium-derived relaxing factors. METHODS AND RESULTS: Insulin resistance was induced in Sprague-Dawley rats by a 4-week fructose-rich diet. Subsequently, mesenteric arteries ( approximately 250 µM) were removed from control and IR rats, and intraluminal diameter was used to assess vascular response to pharmacological probes. Studies with sodium nitroprusside showed that vascular relaxation did not differ between IR and control groups. In contrast, maximal vascular relaxation to acetylcholine (10(-9) to 10(-4) mol/L) in phenylephrine preconstricted arteries was decreased in the IR group (44 +/- 4%) versus control (89 +/- 5%) (P <.01). N-nitro-L-arginine (LNNA) pretreatment further impaired acetylcholine-induced maximal relaxation in the IR group from 44 +/- 4% to 12 +/- 3%; P <.01. In control rats, maximal relaxation was only slightly impaired by the addition of LNNA (89 +/- 5% to 68 +/- 6%; P <.05). The addition of indomethacin to acetylcholine did not affect maximal relaxation in either group. When potassium chloride (KCl) was used fro preconstriction, relaxation to acetylcholine in the IR group was similar to that found with phenylephrine preconstriction (41 +/- 4% v 44 +/- 4%, respectively); however, KCl preconstriction significantly decreased acetyolcholine-induced relaxation in control rats (89 +/- 5% to 43 +/- 5%; P >.01). CONCLUSION: Insulin resistance impairs endothelium-dependent relaxation in small mesenteric arteries. It appears that insulin resistance transforms the primary relaxant factor from endothelial-derived hyperpolarizing factor to nitric oxide. These findings suggest that hypertension and atherosclerosis associated with the IR syndrome are caused, at least in part, by endothelial dysfunction.

Journal Article↗

PubMed1998

Short-term estrogen administration improves abnormal endothelial function in women with systemic sclerosis and Raynaud's phenomenon.

BACKGROUND: Morphologic changes of the vascular endothelium are common in patients with systemic sclerosis and Raynaud's phenomenon. The aim of this study was to evaluate the endothelium-dependent vasodilatation and endothelium-independent vasodilatation and to examine the effects of short-term estrogen administration on vascular responses in these patients. METHODS AND RESULTS: The study included 12 female patients with systemic sclerosis and Raynaud's phenomenon (aged 49+/-14 years) and 12 age- and sex-matched healthy control subjects. With the use of high-resolution ultrasound imaging, brachial artery diameter was measured at rest, during reactive hyperemia (endothelium-dependent response), and after administration of sublingual nitroglycerin (endothelium-independent dilatation). Intima-media thickness of the common carotid artery was also measured. Baseline diameter was similar in patients and control subjects; intima-media thickness was significantly higher in patients (0.83+/-0.3 vs 0.46+/-0.2 mm, P= .002) than in control subjects. Flow-mediated dilatation was reduced in patients (3.6%+/-7% vs 11.9%+/- 4.6%, P = .003); endothelium-independent dilatation also was reduced in patients with Raynaud's phenomenon (14%+/-7% vs 23%+/-6%, P= .003). Vascular responses in 10 patients were examined 15 minutes after administration of conjugated estrogens (25 mg intravenously); there was a significant increase of endothelium-dependent dilatation after estrogen administration (1.7%+/-4% to 6.3%+/-4%, P= .01), whereas endothelium-independent dilatation did not change (13.4%+/-8% to 15.5%+/-7%, not significant). CONCLUSIONS: Endothelium-dependent vasodilatation and endothelium-independent vasodilatation are impaired in patients with Raynaud's phenomenon secondary to systemic sclerosis, whereas intima-media thickness is increased. Short-term estrogen administration can improve endothelial dysfunction in this group of patients.

Adult↗

PubMed2006

Endothelial function and exercise training: evidence from studies using animal models.

This review summarizes and examines the evidence from experiments using animal models to determine the effect of endurance exercise training on endothelium-dependent dilation in the arterial circulation. The response of the endothelium to exercise training is complex and depends on a number of factors that include the duration of the training program, the size of the artery/arteriole, the anatomical location of the artery/arteriole, and the health of the individual. In healthy animals, short-term exercise training appears to cause enhanced endothelium-dependent dilation in some vascular beds, but it returns to normal levels as the duration of the training program increases. In general, evidence supports the notion that exercise training causes greater increases in endothelium-dependent dilation in various disease states than in healthy individuals. The evidence of a generalized effect of training on arterial endothelium in all regions of the body is inconsistent and appears to depend on the animal model used. Available results indicate that training duration, artery size, and anatomical location interact in ways not fully understood at this time to determine whether and to what extent endothelium-dependent dilation will be enhanced by exercise training.

Animals↗

PubMed2006

Vascular neutral endopeptidase inhibition improves endothelial function and reduces intimal hyperplasia.

OBJECTIVE: Neutral endopeptidase (NEP, EC 3.4.24.11) metabolises endogenous vasoactive peptides that may protect against atherogenesis. Since NEP is found in the adventitia of arteries, we investigated the anti-atherogenic effects of chronic adventitial NEP inhibition. METHODS: Intimal hyperplasia of rabbit carotid arteries was induced by placement of soft, non-occlusive, peri-arterial silastic collars. NEP localisation was studied with autoradiography 7 and 14 days after collar placement. Vascular NEP was inhibited in vivo by local superfusion of one collared carotid artery with Candoxatrilat (50 pmol/h), for 7 days (n = 7). The contralateral collar was filled with saline vehicle. After 7 days, ring segments of collared and normal (proximal to the collar) arteries were obtained and in vitro functional measurements, immunohistochemical determination of the pro-atherogenic factor plasminogen activator inhibitor-1 (PAI-1), localization of macrophages and morphometric analyses were carried out. RESULTS: Vascular NEP radiolabelled substrate binding, mainly in the media, was increased by approximately 50% after 7 days (n = 5; p < 0.05) and by approximately 300% after 14 days of collar placement (n = 5; p < 0.05). Compared with normal artery segments from the same animal, vehicle-filled collared sections displayed significantly impaired vasorelaxation to acetylcholine (endothelium-independent vasodilatation was preserved), increased PAI-1 immunostaining, macrophage accumulation and intimal thickening. In Candoxatrilat-treated collared arteries, vasorelaxation to acetylcholine was improved, along with reductions in PAI-1 levels, macrophage numbers and intimal area (all p < 0.05). CONCLUSION: Enhancing the activity of local, endogenous peptides by adventitial inhibition of vascular NEP may protect against early atherogenesis. This is of particular relevance to using adventitial therapies to prevent intimal hyperplasia leading to restenosis.

Acetylcholine↗

PubMed2004

Reduction of infarct size and preservation of endothelial function by multidose intravenous adenosine during extended reperfusion.

It has been proposed that infarct extension is developed from the early to the late phase of reperfusion (R). This study compares the protective effect of single or multidose administration of adenosine (Ado) on infarct size during early and late phases of R by attenuating neutrophil (PMN) recruitment. Forty-one dogs underwent 60-min left anterior descending artery (LAD) ischemia followed by 6, 24, and 48 h of R, respectively. Infarct size (%) increased over 6 to 24 h (27 +/- 2 to 38 +/- 4; P < 0.05 24 h versus 6 h group), with a corresponding increase in creatine kinase activity. Transmural myocardial blood flow (mL/min/g) decreased from 6 to 24 h (0.47 +/- 0.02 to 0.29 +/- 0.02; P < 0.05 24 h versus 6 h group). PMN localization (mm(2) myocardium) in the perinecrotic tissue detected by immunohistochemistry with anti-CD18 antibody, and accumulation detected by myeloperoxidase (MPO, DeltaAbs/min/g) increased from 6 to 24 h (292 +/- 25 to 605 +/- 44; P < 0.05 24 h versus 6 h group; and 55 +/- 7 to 96 +/- 5; P < 0.05 24 h versus 6 h group), respectively. In in vitro analysis, PMN adherence (mm(2) endothelium) to postischemic LAD increased from 98 +/- 2 to 125 +/- 3 (P < 0.05 24 h versus 6 h group) and maximal LAD endothelium-dependent relaxation (%) impaired from 6 to 24 h (74 +/- 7 to 42 +/- 10; P < 0.05 24 h versus 6 h group). Intravenous Ado (140 microg/kg/min) for 2 h at R reduced infarct size (17 +/- 2; P < 0.05 Ado versus 6 h group), CD18 positive cells (130 +/- 10; P < 0.05 Ado versus 6 h group), MPO (14 +/- 3; P < 0.05 Ado versus 6 h group), PMN adherence (57 +/- 2; P < 0.05 Ado versus 6 h group), and augmented LAD vascular relaxation (102 +/- 5 versus 74 +/- 7; P < 0.05 Ado versus 6 h group). However, this protection by Ado was lost when R was extended to 24 h. Treatment with multiple infusion of Ado at 2, 6, 12, and 18 h R significantly preserved protective effects seen at 6 h R in the Ado group. Protection by multidose Ado was still preserved when R was extended to an additional 24 h. These data suggest that interventions aiming at permanently reducing R injury may thus need to be administered not only at early R, but also during late phase. A slow wave of PMN accumulation at late R may be involved in the extension of infarction and endothelial dysfunction.

Adenosine↗

PubMed1999