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Daniel J. Green - One of the best experts on this subject based on the ideXlab platform.
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relationship between monocyte platelet aggregation and Endothelial Function in middle aged and elderly adults
Physiological Reports, 2017Co-Authors: Andrew Haynes, Daniel J. Green, Matthew D Linden, Elisa Robey, Louise H Naylor, Kay L Cox, Nicola T LautenschlagerAbstract:Low-grade inflammation, Endothelial dysFunction, and platelet hyper-reactivity to agonists are associated with an increased risk of cardiovascular events. In vitro and animal studies infer an inverse mechanistic relationship between platelet activation and the production of endothelium-derived nitric oxide and prostacyclin. This concept is supported by evidence of an inverse relationship between Endothelial Function and platelet activation in high-risk cardiac patients. The aim of this study was to investigate what relationship, if any, exists between platelet and Endothelial Function in healthy, middle-aged, and elderly adults. In 51 participants (18 male, 33 post menopausal female), Endothelial Function was assessed by flow-mediated dilation (FMD). Platelet Function was assessed by flow cytometric determination of glycoprotein IIb/IIIa activation (measured by PAC-1 binding), granule exocytosis (measured by surface P-selectin expression), and monocyte-platelet aggregates (MPAs), with and without stimulation by canonical platelet agonists adenosine diphosphate (ADP), arachidonic acid (AA), and collagen. Correlation analysis indicated there was no significant (all P => 0.05) relationship between FMD and any marker of in vivo platelet activation (MPAs R = 0.193, PAC-1 R = -0.113, anti-CD62P R = -0.078) or inducible platelet activation by ADP (MPA R = -0.128, anti-CD62P R = -0.237), AA (MPA R = -0.122, PAC-1 R = -0.045, anti-CD62P R = -0.142), or collagen (MPA R = 0.136, PAC-1 R = 0.174, anti-CD62P R = -0.077). Our findings contrast with two previous studies performed in high-risk cardiac patients, which reported inverse relationships between platelet activation and Endothelial Function, suggesting that some compensatory redundancy may exist in the relationship between platelet and Endothelial Function in preclinical populations.
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retrograde flow and shear rate acutely impair Endothelial Function in humans
Hypertension, 2009Co-Authors: Dick H. J. Thijssen, Toni M Tinken, Ellen A. Dawson, Timothy N Cable, Daniel J. GreenAbstract:Changes in arterial shear stress induce Functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on Endothelial Function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated Endothelial Function, in healthy men (243 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in "dose"-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of Endothelial Function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo. (Hypertension. 2009;53:986-992.)
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losartan an angiotensin type 1 receptor antagonist improves Endothelial Function in non insulin dependent diabetes
Journal of the American College of Cardiology, 2000Co-Authors: Craig Cheetham, Daniel J. Green, Julie Collis, G Odriscoll, K Stanton, R R TaylorAbstract:OBJECTIVES The present study examined the effect on forearm Endothelial Function of an angiotensin II type 1 receptor antagonist, losartan, in subjects with non-insulin-dependent diabetes mellitus (NIDDM). BACKGROUND Angiotensin-converting enzyme (ACE) inhibition with enalapril improves acetylcholine (ACh)-dependent Endothelial Function in patients with NIDDM. This could be mediated through angiotensin II and the type 1 receptor or could be due to inhibition of kininase II and a bradykinin preserving effect. It is therefore relevant to determine whether a type 1 receptor antagonist improves Endothelial Function. METHODS The influence of losartan (50 mg daily for four weeks) on endothelium-dependent and independent vasodilator Function was determined in 9 NIDDM subjects using a double-blinded placebo-controlled crossover protocol. Forearm blood flow was measured using strain-gauge plethysmography. RESULTS Losartan significantly decreased infused arm vascular resistance in response to three incremental doses of intrabrachial acetylcholine (p < 0.05, ANOVA). The forearm blood flow ratio (flow in infused to noninfused arm) was also increased (p < 0.01). Responses to sodium nitroprusside and monomethyl arginine were not significantly changed. CONCLUSIONS Losartan administration at 50 mg per day improved endothelium-dependent dilation of resistance vessels in patients with NIDDM. That is, blockade of the angiotensin II type 1 receptors improves Endothelial Function in NIDDM. At least some of the similarly beneficial effect of ACE inhibition is probably mediated also through the angiotensin II-type 1 receptor pathway. The use of a type 1 receptor antagonist seems a reasonable alternative to an ACE inhibitor to maintain Endothelial Function in NIDDM subjects.
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improvement in Endothelial Function by angiotensin converting enzyme inhibition in insulin dependent diabetes mellitus
Journal of Clinical Investigation, 1997Co-Authors: G Odriscoll, Daniel J. Green, K Stanton, James M Rankin, R R TaylorAbstract: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.
Amir Lerman - One of the best experts on this subject based on the ideXlab platform.
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effect of metformin on microvascular Endothelial Function in polycystic ovary syndrome
Mayo Clinic proceedings, 2019Co-Authors: Behnam Heidari, Amir Lerman, Antigoni Z Lalia, Lilach O Lerman, Alice Y ChangAbstract:Abstract Objective To investigate the factors that are associated with the effect of metformin on Endothelial dysFunction in polycystic ovary syndrome (PCOS). Patients and Methods From March 24, 2014, to November 18, 2016, 48 women with PCOS were randomly assigned to 1500 mg/d of metformin (N=29) or no treatment (N=13) for 3 months; 42 patients (29 in the initial treatment group and 13 in the no treatment group) completed the study. Study variables were measured at baseline and after 3 months. Participants who did not receive metformin initially were then treated with metformin for another 3 months, and study variables were measured again. Endothelial Function was measured as reactive hyperemia–peripheral arterial tonometry (RH-PAT) from the index finger. Results The age and baseline Endothelial Function (mean ± SD) of the participants were 32.7±6.9 years and 1.8±0.5, respectively. No notable change was observed in Endothelial Function after 3 months with metformin compared with no treatment. However, after stratifying participants who received metformin based on baseline Endothelial Function, there was a significant improvement following metformin treatment in participants with abnormal baseline Endothelial Function (1.3±0.3 vs 1.7±0.3; P Conclusion Metformin improves Endothelial Function in women with PCOS and Endothelial dysFunction independent of changes in glucose metabolism, dyslipidemia, or presence of prediabetes. Metformin has a direct effect on Endothelial Function in PCOS, and measurement of Endothelial Function can stratify and follow response to metformin treatment in PCOS. Trial Registration clinicaltrials.gov Identifier: NCT02086526 .
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abstract 12145 effect of metformin on microvascular Endothelial Function in polycystic ovary syndrome
Circulation, 2018Co-Authors: Behnam Heidari, Lilach O Lerman, Alice Y Change, Amir LermanAbstract:Background: Polycystic Ovary Syndrome (PCOS) is associated with increased prevalence of cardiovascular risk factors. Endothelial Function (EF) is an important index of subclinical atherosclerosis, ...
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Endothelial Function cardiac events
Circulation, 2005Co-Authors: Amir Lerman, Andreas M ZeiherAbstract:A growing body of evidence suggests that Endothelial dysFunction is associated with cardiovascular events. Endothelial dysFunction can be regarded as a syndrome that exhibits systemic manifestations associated with significant morbidity and mortality. The concept of Endothelial dysFunction should be extended beyond the conduit vessels into the vascular wall and even to the bone marrow and the progenitor Endothelial cells. The present review is focused on the potential underlying mechanism by which Endothelial dysFunction may contribute to cardiovascular events. The assessment of Endothelial Function may emerge as an integral adjuvant test for evaluation of the vulnerable patients at risk for future cardiovascular events. Atherosclerosis is a chronic, systemic, and diffuse disease with focal complications in different vascular beds. The mechanisms by which a specific site is rendered more prone to the development of symptomatic disease and cardiovascular events are not known. The observation that all stages of atherosclerosis may be at distant and at multiple locations simultaneously but at the same time may spare entire segments may give rise to the hypothesis that the interface and interaction between the vascular wall and the circulation is the primary site of the mechanism underlying cardiovascular events.1 The endothelium is the monolayer of Endothelial cells lining the lumen of the vascular beds and is mechanically and metabolically strategically located, separating the vascular wall from the circulation and the blood components.1,2 To fully understand the mechanism by which alteration in Endothelial Function may lead to cardiovascular events, we need to extend our vision and concepts regarding the nature and Function of the endothelium. ### Localization and Distribution of the Endothelium The first concept that needs to be revised is the localization and distribution of the Endothelial cell layer. The focus in the past decade has been on the Endothelial layer of the large conduit vessels and the vascular lumen.2 …
Behnam Heidari - One of the best experts on this subject based on the ideXlab platform.
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effect of metformin on microvascular Endothelial Function in polycystic ovary syndrome
Mayo Clinic proceedings, 2019Co-Authors: Behnam Heidari, Amir Lerman, Antigoni Z Lalia, Lilach O Lerman, Alice Y ChangAbstract:Abstract Objective To investigate the factors that are associated with the effect of metformin on Endothelial dysFunction in polycystic ovary syndrome (PCOS). Patients and Methods From March 24, 2014, to November 18, 2016, 48 women with PCOS were randomly assigned to 1500 mg/d of metformin (N=29) or no treatment (N=13) for 3 months; 42 patients (29 in the initial treatment group and 13 in the no treatment group) completed the study. Study variables were measured at baseline and after 3 months. Participants who did not receive metformin initially were then treated with metformin for another 3 months, and study variables were measured again. Endothelial Function was measured as reactive hyperemia–peripheral arterial tonometry (RH-PAT) from the index finger. Results The age and baseline Endothelial Function (mean ± SD) of the participants were 32.7±6.9 years and 1.8±0.5, respectively. No notable change was observed in Endothelial Function after 3 months with metformin compared with no treatment. However, after stratifying participants who received metformin based on baseline Endothelial Function, there was a significant improvement following metformin treatment in participants with abnormal baseline Endothelial Function (1.3±0.3 vs 1.7±0.3; P Conclusion Metformin improves Endothelial Function in women with PCOS and Endothelial dysFunction independent of changes in glucose metabolism, dyslipidemia, or presence of prediabetes. Metformin has a direct effect on Endothelial Function in PCOS, and measurement of Endothelial Function can stratify and follow response to metformin treatment in PCOS. Trial Registration clinicaltrials.gov Identifier: NCT02086526 .
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abstract 12145 effect of metformin on microvascular Endothelial Function in polycystic ovary syndrome
Circulation, 2018Co-Authors: Behnam Heidari, Lilach O Lerman, Alice Y Change, Amir LermanAbstract:Background: Polycystic Ovary Syndrome (PCOS) is associated with increased prevalence of cardiovascular risk factors. Endothelial Function (EF) is an important index of subclinical atherosclerosis, ...
Nigel Benjamin - One of the best experts on this subject based on the ideXlab platform.
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effect of dietary nitrate on blood pressure Endothelial Function and insulin sensitivity in type 2 diabetes
Free Radical Biology and Medicine, 2013Co-Authors: Mark Gilchrist, Paul G. Winyard, Christine Anning, Angela C. Shore, Kunihiko Aizawa, Nigel BenjaminAbstract:Diets rich in green, leafy vegetables have been shown to lower blood pressure (BP) and reduce the risk of cardiovascular disease. Green, leafy vegetables and beetroot are particularly rich in inorganic nitrate. Dietary nitrate supplementation, via sequential reduction to nitrite and NO, has previously been shown to lower BP and improve Endothelial Function in healthy humans. We sought to determine if supplementing dietary nitrate with beetroot juice, a rich source of nitrate, will lower BP and improve Endothelial Function and insulin sensitivity in individuals with type 2 diabetes (T2DM). Twenty-seven patients, age 67.2±4.9 years (18 male), were recruited for a double-blind, randomized, placebo-controlled crossover trial. Participants were randomized to begin, in either order, a 2-week period of supplementation with 250ml beetroot juice daily (active) or 250ml nitrate-depleted beetroot juice (placebo). At the conclusion of each intervention period 24-h ambulatory blood pressure monitoring, tests of macro- and microvascular Endothelial Function, and a hyperinsulinemic isoglycemic clamp were performed. After 2 weeks administration of beetroot juice mean ambulatory systolic BP was unchanged: 134.6±8.4mmHg versus 135.1±7.8mmHg (mean±SD), placebo vs active-mean difference of -0.5mmHg (placebo-active), p=0.737 (95% CI -3.9 to 2.8). There were no changes in macrovascular or microvascular Endothelial Function or insulin sensitivity. Supplementation of the diet with 7.5mmol of nitrate per day for 2 weeks caused an increase in plasma nitrite and nitrate concentration, but did not lower BP, improve Endothelial Function, or improve insulin sensitivity in individuals with T2DM.
R R Taylor - One of the best experts on this subject based on the ideXlab platform.
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losartan an angiotensin type 1 receptor antagonist improves Endothelial Function in non insulin dependent diabetes
Journal of the American College of Cardiology, 2000Co-Authors: Craig Cheetham, Daniel J. Green, Julie Collis, G Odriscoll, K Stanton, R R TaylorAbstract:OBJECTIVES The present study examined the effect on forearm Endothelial Function of an angiotensin II type 1 receptor antagonist, losartan, in subjects with non-insulin-dependent diabetes mellitus (NIDDM). BACKGROUND Angiotensin-converting enzyme (ACE) inhibition with enalapril improves acetylcholine (ACh)-dependent Endothelial Function in patients with NIDDM. This could be mediated through angiotensin II and the type 1 receptor or could be due to inhibition of kininase II and a bradykinin preserving effect. It is therefore relevant to determine whether a type 1 receptor antagonist improves Endothelial Function. METHODS The influence of losartan (50 mg daily for four weeks) on endothelium-dependent and independent vasodilator Function was determined in 9 NIDDM subjects using a double-blinded placebo-controlled crossover protocol. Forearm blood flow was measured using strain-gauge plethysmography. RESULTS Losartan significantly decreased infused arm vascular resistance in response to three incremental doses of intrabrachial acetylcholine (p < 0.05, ANOVA). The forearm blood flow ratio (flow in infused to noninfused arm) was also increased (p < 0.01). Responses to sodium nitroprusside and monomethyl arginine were not significantly changed. CONCLUSIONS Losartan administration at 50 mg per day improved endothelium-dependent dilation of resistance vessels in patients with NIDDM. That is, blockade of the angiotensin II type 1 receptors improves Endothelial Function in NIDDM. At least some of the similarly beneficial effect of ACE inhibition is probably mediated also through the angiotensin II-type 1 receptor pathway. The use of a type 1 receptor antagonist seems a reasonable alternative to an ACE inhibitor to maintain Endothelial Function in NIDDM subjects.
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improvement in Endothelial Function by angiotensin converting enzyme inhibition in insulin dependent diabetes mellitus
Journal of Clinical Investigation, 1997Co-Authors: G Odriscoll, Daniel J. Green, K Stanton, James M Rankin, R R TaylorAbstract: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.