Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

Magen, Eli; Viskoper, J. R.; Mishal, Joseph; Priluk, R.; London, Daniel A.; Yosefy, Chaim

doi:10.1038/sj.jhh.1001910

Cited by 47 publications

(45 citation statements)

References 33 publications

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“…Evidence from explorative clinical trials suggests that treatment with low-dose aspirin increases EDR. In humans, low-dose aspirin administered over a 2-mo period has been found to improve endothelial function (34). In rats with vascular endothelial injury induced by an injection of native LDL, low-dose aspirin is able to reverse the EDR dysfunction (11).…”

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confidence: 99%

Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging

Bulckaen¹,

Prévost²,

Boulanger³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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The age-related impairment of endothelium-dependent vasodilatation contributes to increased cardiovascular risk in the elderly. For primary and secondary prevention, aspirin can reduce the incidence of cardiovascular events in this patient population. The present work evaluated the effect of low-dose aspirin on age-related endothelial dysfunction in C57B/J6 aging mice and investigated its protective antioxidative effect. Agerelated endothelial dysfunction was assessed by the response to acetylcholine of phenylephrine-induced precontracted aortic segments isolated from 12-, 36-, 60-, and 84-wk-old mice. The effect of low-dose aspirin was examined in mice presenting a decrease in endothelial-dependent relaxation (EDR). The effects of age and aspirin treatment on structural changes were determined in mouse aortic sections. The effect of aspirin on the oxidative stress markers malondialdehyde and 8-hydroxy-2Ј-deoxyguanosine (8-OhdG) was also quantified. Compared with that of 12-wk-old mice, the EDR was significantly reduced in 60-and 84-wk-old mice (P Ͻ 0.05); 68-wkold mice treated with aspirin displayed a higher EDR compared with control mice of the same age (83.9 Ϯ 4 vs. 66.3 Ϯ 5%; P Ͻ 0.05). Aspirin treatment decreased 8-OHdG levels (P Ͻ 0.05), but no significant effect on intima/media thickness ratio was observed. The protective effect of aspirin was not observed when treatment was initiated in older mice (96 wk of age). It was found that low-dose aspirin is able to prevent age-related endothelial dysfunction in aging mice. However, the absence of this effect in the older age groups demonstrates that treatment should be initiated early on. The underlying mechanism may involve the protective effect of aspirin against oxidative stress. endothelium; intima/media; vasodilatation; oxidative stress AGE-ASSOCIATED CHANGES SUCH as endothelial dysfunction are involved in the significantly increased risk of cardiovascular complications and microthrombus formation in the elderly patient population (44). The presence of endothelial dysfunction in the coronary or peripheral circulation has been shown to constitute a risk factor for cardiovascular events independent of the development of atherosclerosis or other vascular risk factors (22,(43)(44)(45). There is emerging evidence that age-associated endothelial dysfunction is related to the local formation of reactive oxygen and nitrogen species within and in the vicinity of the vascular wall (13,25,36,43,49). Therapeutic approaches capable of preventing or reversing age-related endothelial dysfunction may thus help to reduce cardiovascular risk in the elderly.Age-related endothelial-dependent relaxation (EDR) decreases in the large vessels of different animal species including humans (36). EDR in response to acetylcholine (ACh) decreases with age in the rat aorta: the maximal relaxation effect of ACh is 100% in 4-to 6-wk-old, 50% in 3-to 6-mo-old, and 25% in 12-to 25-mo-old rats (29). The agerelated decrease in EDR varies from one vessel to another and from one species to anot...

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confidence: 99%

Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging

Bulckaen¹,

Prévost²,

Boulanger³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…22,23 On the other hand, Hermida et al reported an inverse association between aspirin intake (100 mg/day) given before bed-time and mean 24 hour BP levels (-6/-4 mm Hg reduction of systolic BP/ diastolic BP) 10 especially in non-dippers. 11 24 Two meta-analyses assessing the association of aspirin and other NSAIDs with BP levels have been published. The first meta-analysis found that among a total of 771 participants, NSAIDs increased mean blood pressure by 5 mm Hg overall (95% CI, 1.2-8.7).…”

Section: Discussionmentioning

confidence: 99%

Aspirin, Non-Aspirin Analgesics and the Risk of Hypertension in the SUN Cohort

Beunza

Martínez‐González

Bes–Rastrollo

et al. 2010

Revista Española de Cardiología (English Edition)

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Introduction and objectives. The use of aspirin and non-aspirin analgesics have been associated with changes in blood pressure. The aim of this study was to investigate prospectively the association between the regular use of aspirin and non-aspirin analgesics and the incidence of hypertension.Methods. The SUN project is an ongoing, continuously expanding, prospective cohort of Spanish university graduates initially free of hypertension, cardiovascular disease, diabetes, and cancer; 9986 (mean age, 36 years) were recruited during 1999-2005 and followed up for a mean of 51 months. Regular aspirin and non-aspirin analgesic use and the presence of other risk factors for hypertension were assessed by questionnaire at baseline, and the incidence of hypertension was assessed using biennial follow-up questionnaires.Results. In total, 543 new cases of hypertension were identified during follow-up. Regular aspirin use (ie, ≥2 days/ week) was associated with a higher risk of hypertension (hazard ratio = 1.45; 95% confidence interval, 1.02-2.04) after adjustment for various confounding factors. Regular use of non-aspirin analgesic drugs was also associated with a higher risk of hypertension (hazard ratio = 1.69; 95% confidence interval, 1.28-2.23).Conclusions. The regular use of aspirin and non-aspirin analgesics were both associated with an increased risk of developing hypertension, independently of other risk factors. Aspirina, analgésicos y riesgo de hipertensión arterial en la Cohorte SUN Introducción y objetivos. Se ha relacionado el consumo de aspirina y de otros analgésicos con cambios en la presión arterial. El objetivo de nuestro estudio fue valorar prospectivamente la asociación del uso habitual de aspirina y otros analgésicos con la incidencia de hipertensión arterial.Métodos. El proyecto SUN es una cohorte prospectiva y dinámica que incluyó a 9.986 graduados universitarios españoles inicialmente libres de hipertensión, enfermedad cardiovascular, diabetes o cáncer (media de edad, 36 años). Fueron reclutados durante el periodo 1999-2005 y se los siguió prospectivamente durante una media de 51 meses. El uso habitual de aspirina y otros analgési-cos, así como la presencia de otros factores de riesgo de hipertensión arterial, se valoró mediante un cuestionario basal. La incidencia de hipertensión se valoró con cuestionarios de seguimiento bienales.Resultados. Durante el seguimiento se identificaron 543 casos nuevos de hipertensión arterial. El uso habitual de aspirina (2 o más días/semana) se asoció con un mayor riesgo de hipertensión (hazard ratio [HR] = 1,45; intervalo de confianza [IC] del 95%, 1,02-2,04) tras ajustar por diversos factores de confusión. El uso habitual de otros analgésicos diferentes de la aspirina también se asoció a un mayor riesgo de hipertensión arterial (HR = 1,69; IC del 95%, 1,28-2,23).Conclusiones. El uso habitual tanto de aspirina como de otros analgésicos diferentes a la aspirina parece asociarse a mayor riesgo de hipertensión arterial, independientemente de otros factores de riesgo.

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“…Indeed, use of simple drugs such as aspirin may influence endothelial function in hypertension. 3,4 Endothelial cells also facilitate the transport of glucose by GLUT, 5 mainly present in brain barrier, of amino acids (such as L-arginine, a substrate for nitric oxide (NO)). Recent data even suggest a relationship of the endothelium to angiogenesis.…”

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confidence: 99%

Insights into human hypertension: the role of endothelial dysfunction

Giansante

Fiotti

2005

J Hum Hypertens

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Atherosclerosis is considered an ubiquitous pathological process. In patients symptomatic for coronary artery or carotid or peripheral arterial disease, other localizations -still asymptomatic -of atherosclerotic lesions are often found. Despite this consideration, the patterns of arteries developing atherosclerosis can be quite diverse: for example, lesions prevalently develop in regions where the flow is either low or turbulent such as where artery bifurcates, mammalian artery are nearly unaffected by atherosclerosis. 1 So, what makes the difference? The answer probably lies in the marked phenotypic variation between endothelial cells in the different vascular locations, and in the different responses of the vascular layers to the same stimulus in the same individual, as well.Indeed, the vascular endothelium, once believed to be an inert edge between artery and blood, is now recognized as an organ per se. 2 Many studies over the past 10 years indicate that endothelial cells have important transport functions, act as the provision of an antithrombogenic interface, control of platelet adherence and thrombosis, as well as active actions in inflammation and vascular tone. Indeed, use of simple drugs such as aspirin may influence endothelial function in hypertension. 3,4 Endothelial cells also facilitate the transport of glucose by GLUT, 5 mainly present in brain barrier, of amino acids (such as L-arginine, a substrate for nitric oxide (NO)). Recent data even suggest a relationship of the endothelium to angiogenesis. 6 In addition, hypertensive patients with diabetes mellitus have endothelial dysfunction that can be related to urinary albumin excretion and inflammation, as well as modified by antihypertensive therapy. [7][8][9] Of note, endothelial cells may be actively involved in inflammation through the expression of Toll-like receptors -4 and -2, leading to increased expression of inflammation mediators such as chemokines, adhesion molecules and metalloproteinase. 10 Finally, endothelial cells are also intimately involved in haemostasis and coagulation by the production of substances such as tissue factor pathway inhibitor, thrombomodulin, endothelial protein C receptor and von Willebrand factor. 5 Of particular interest, in the pathophysiology of the endothelium, is the endothelial regulation of vascular tone. 2 Endothelial cells produce several vasoactive substances, and among them is NO, the most powerful vasodilator. 2 NO is produced by endothelial cells via NOS III (eNOS) or via NOS II (iNOSII), where the former is constitutive and acts to maintain the vascular musculature in a state of vasodilatation, while the latter is inducible by immunological stimuli. 2,11 Indeed, several studies have demonstrated that low NO, whose circulating levels are considered as a surrogate of endothelial dysfunction, is an early marker in patients with common cardiovascular risk factors, such as diabetes, smoking and hypertension. 2 In a recent issue of the Journal of Human Hypertension, Srivastava et al. 12 confirm that in p...

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Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

Cited by 47 publications

References 33 publications

Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging

Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging

Aspirin, Non-Aspirin Analgesics and the Risk of Hypertension in the SUN Cohort

Insights into human hypertension: the role of endothelial dysfunction

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