Large and small artery endothelial function in patients with essential hypertension – Effect of ACE inhibition and beta‐blockade

Buus, Niels Henrik; Jørgensen, Claus G.; Mulvany, Michael J.; Sørensen, Keld E.

doi:10.1080/08037050701343688

Cited by 18 publications

(6 citation statements)

References 41 publications

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“…This was a homogeneous population without known risk factors. In reality, patients with chronic diseases would be on medications, some of which have antiinflammatory effects (Buus et al, 2007;Mäki-Petäjä et al, 2007). Further studies need to be performed on such subjects to observe any possible coffeedisease interaction on endothelial function.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of coffee on endothelial function in healthy subjects

et al. 2010

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Background/Objectives: Coffee is the most widely consumed beverage in the world, but its effect on the cardiovascular system has not been fully understood. Coffee contains caffeine and antioxidants, which may influence endothelial function, both of which have not yet been investigated. The objective of this study was to investigate the acute effects of coffee on endothelial function measured by brachial artery flow-mediated dilation (FMD). Subjects/Methods: A total of 20 (10 males and 10 females) healthy non-obese subjects underwent a double-blind, crossover study. Subjects ingested one cup of caffeinated (CC) and one cup of decaffeinated (DC) Italian espresso coffee in random order at 5-to 7-day intervals. Results: Following CC ingestion, FMD decreased progressively and significantly (mean±s.e.m.: 0 min, 7.7±0.6; 30 min, 6.3 ± 0.7; 60 min, 6.0 ± 0.8%; ANOVA (analysis of variance), Po0.05), but it did not significantly increase after DC ingestion (0 min, 6.9±0.6; 30 min, 8.1±0.9; 60 min, 8.5±0.9%; P ¼ 0.115). Similarly, CC significantly increased both systolic and diastolic blood pressure; this effect was not observed after DC ingestion. Blood glucose concentrations remained unchanged after ingestion of both CC and DC, but insulin (0 min, 15.8±0.9; 60 min, 15.0±0.8 mU/ml; Po0.05) and C-peptide (0 min, 1.25 ± 0.09; 60 min, 1.18 ± 0.09 ng/ml; Po0.01) blood concentrations decreased significantly only after CC ingestion. Conclusions: CC acutely induced unfavorable cardiovascular effects, especially on endothelial function. In the fasting state, insulin secretion is also likely reduced after CC ingestion. Future studies will determine whether CC has detrimental clinically relevant effects, especially in unhealthy subjects.

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Section: Discussionmentioning

confidence: 99%

Acute effects of coffee on endothelial function in healthy subjects

et al. 2010

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“…34 No difference between medications was observed. The increase in the percentage of dilation after 1 year of treatment was inversely correlated with change with treatment in the rCBF response during working memory in all of the ROIs (r: Ϫ0.50 to Ϫ0.68; PՅ0.01).…”

Section: Peripheral Vasodilative Effectsmentioning

confidence: 94%

Cerebrovascular Support for Cognitive Processing in Hypertensive Patients Is Altered by Blood Pressure Treatment

et al. 2008

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Abstract-Hypertension is associated with mild decrements in cognition. In addition, regional cerebral blood flow responses during memory processing are blunted in parietal and thalamic areas among untreated hypertensive adults, who, compared with normotensive subjects, manifest greater correlation in blood flow response across task-related brain regions. Here, we test whether pharmacological treatment of hypertension normalizes regional cerebral blood flow responses and whether it does so differentially according to drug class. Treatment with lisinopril, an angiotensinconverting enzyme blocker, known to enhance vasodilative responsivity, was compared with treatment with atenolol, a ␤-blocker. Untreated hypertensive volunteers (nϭ28) were randomly assigned and treated for 1 year. Whole brain and regional cerebral flow responses to memory processing and acutely administered acetazolamide, a vasodilator, were assessed pretreatment and posttreatment. Peripheral brachial artery dilation during reactive hyperemia was also measured. Quantitative blood flow measures showed no difference in the magnitude of regional cerebral blood flow responses pretreatment and posttreatment to either memory tasks or acetazolamide injection. Brachial artery flow-mediated dilation increased with treatment. No differences between medications were observed. In brain regions active in memory processing, however, regional cerebral blood flow responses were more highly correlated after treatment. Specificity of cerebral blood flow to different regions appears to decline with treatment of hypertension. This greater correlation among active brain regions, which is present as well in untreated hypertensive relative to normotensive volunteers, may represent compensation in the face of less region-specific responsivity in individuals with hypertension. M ild-to-moderate hypertension is associated with minor deficits in cognition. [1][2][3][4] Brain structure or function might account for these deficits. [5][6][7][8] Cognitive processing elicits a regional redistribution of blood flow, providing metabolic support to active neural areas. 9 Interference with this redistribution, blunting of regional blood flow, or structural loss because of poor perfusion might underlie the deficits of hypertensive individuals. Limited existing evidence supports all of these possibilities. [5][6][7][8]10 We demonstrated that, compared with normotensive individuals, those with hypertension have damped regional cerebral blood flow (CBF; rCBF) responses in parietal and thalamic areas (regions of interest [ROI]) during working memory tasks and greater correlation among rCBF responses across task-related regions. 7 Both observations might be because of a cerebrovascular adaptation to hypertension, most particularly, the remodeling of walls of small arteries, ie, thickening of the medial layer with or without a change in lumen diameter. 7 Antihypertensive medications have established influences on peripheral vascular function and may have similar effects on cerebrovascular...

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“…23 Accordingly, increased ATII concentrations, along with increased levels of superoxide anions, have been shown in the shoulder region of atherosclerotic plaques. 67 In line with a role of ATII in endothelial dysfunction and hypertension, numerous studies have now demonstrated that the therapy with angiotensin-converting enzyme inhibitors and AT-1 receptor blockers is associated with an improvements in endothelial responsiveness [68][69][70][71][72] (the existence of negative reports also needs to be acknowledged). 73 In animal models of ATII-induced hypertension, 14 increased ROS production by Nox was also associated with eNOS uncoupling.…”

Section: Ros Sources In Hypertension Nadph Oxidasesmentioning

confidence: 98%

Oxidative stress and endothelial dysfunction in hypertension

2011

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Systemic arterial hypertension is a highly prevalent cardiovascular risk factor that causes significant morbidity and mortality, and is becoming an increasingly common health problem because of the increasing longevity and prevalence of predisposing factors such as sedentary lifestyle, obesity and nutritional habits. Further complicating the impact of this disease, mild and moderate hypertension are usually asymptomatic, and their presence (and the subsequent increase in cardiovascular risk) is often unrecognized. The pathophysiology of hypertension involves a complex interaction of multiple vascular effectors including the activation of the sympathetic nervous system, of the renin-angiotensin-aldosterone system and of the inflammatory mediators. Subsequent vasoconstriction and inflammation ensue, leading to vessel wall remodeling and, finally, to the formation of atherosclerotic lesions as the hallmark of advanced disease. Oxidative stress and endothelial dysfunction are consistently observed in hypertensive subjects, but emerging evidence suggests that they also have a causal role in the molecular processes leading to hypertension. Reactive oxygen species (ROS) may directly alter vascular function or cause changes in vascular tone by several mechanisms including altered nitric oxide (NO) bioavailability or signaling. ROS-producing enzymes involved in the increased vascular oxidative stress observed during hypertension include the NADPH oxidase, xanthine oxidase, the mitochondrial respiratory chain and an uncoupled endothelial NO synthase. In the current review, we will summarize our current understanding of the molecular mechanisms in the development of hypertension with an emphasis on oxidative stress and endothelial dysfunction.

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Large and small artery endothelial function in patients with essential hypertension – Effect of ACE inhibition and beta‐blockade

Cited by 18 publications

References 41 publications

Acute effects of coffee on endothelial function in healthy subjects

Acute effects of coffee on endothelial function in healthy subjects

Cerebrovascular Support for Cognitive Processing in Hypertensive Patients Is Altered by Blood Pressure Treatment

Oxidative stress and endothelial dysfunction in hypertension

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