Effect of the renin–angiotensin system on the vessel wall: using ACE inhibition to improve endothelial function

Neutel, Joel M.

doi:10.1038/sj.jhh.1001714

Cited by 45 publications

(32 citation statements)

References 38 publications

(46 reference statements)

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“…Clinical evaluation of vascular damage is performed through study of changes in: (1) intimal medial thickness (IMT) of carotid arteries during carotid duplex ultrasound examination; (2) vascular endothelial function and (3) arterial compliance. At equal degrees of reduction in blood pressure, RAS inhibitors produced a greater reduction in carotid IMT, 36,37 greater improvement in vascular endothelial function assessed non-invasively by flow mediated dilatation in brachial artery 18,38 and in arterial compliance 18,39 when compared with other antihypertensive agents.…”

Section: Benefits Of Ras Inhibitors Beyond Blood Pressure Loweringmentioning

confidence: 96%

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RAS inhibition in hypertension

Ibrahim

2006

J Hum Hypertens

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Section: Benefits Of Ras Inhibitors Beyond Blood Pressure Loweringmentioning

confidence: 96%

“…Agents with high T/P are perindopril, lisinopril and trandolapril. 18 While the significance of the T/P of ACE-Is have not been evaluated in clinical outcome studies, consistent effective control over the entire 24 h period is desirable.…”

Section: Antihypertensive Responsementioning

confidence: 99%

RAS inhibition in hypertension

Ibrahim

2006

J Hum Hypertens

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“…13 Indeed, many strategies have also been used to correct reduced synthesis or increased degradation of NO in many pathological conditions, such as heart failure. 14 To increase the availability of NO, a supplementation of L-arginine -the substrate for NO synthesis -has been administered in patients with heart failure, and a beneficial effect was found in the 6-min walk test. Another therapeutic approach consists in administering a direct donor of NO -nitroglycerin -but with more controversial results.…”

Section: No Is Produced By Endothelial Cells Via Nos III (Enos) or Vimentioning

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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“…25 While the role of angiotensin receptor blockers is well established in treating hypertension, further research is underway to evaluate the role of these agents in primary prevention of hypertension by suppressing the inflammatory state or by prevent endothelial dysfunction. 26 Finally, oxidation of low-density lipoproteins by oxygen-free radicals may increase hypertension-related atherogenesis -perhaps via endothelial damage/dysfunction -and antioxidants may be beneficial in this regard. 27 A discussion on new insights into the pathogenesis of hypertension cannot fail to mention genes.…”

mentioning

confidence: 99%