Angiotensin-Converting Enzyme Inhibition Restores Flow-Dependent and Cold Pressor Test–Induced Dilations in Coronary Arteries of Hypertensive Patients

Antony, Isabelle; Lerebours, Guy; Nitenberg, A

doi:10.1161/01.cir.94.12.3115

Cited by 116 publications

(61 citation statements)

References 58 publications

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“…Abundant amounts of ACE are present in endothelial cells, and ACE-I have been shown to improve coronary artery endothelial function. 37,[42][43][44] Thrombosis and platelet aggregation in coronary vessels is also modulated by Ang II, and there is evidence that ACE-I improve the fibrinolytic balance. 45 A major substudy of the EUROPA trial, PERTINENT trial (PERindopril Thrombosis InflammatioN Endothelial dysfunction and Neurohormonal activation), should provide additional information in this area.…”

Section: Baselinementioning

confidence: 99%

Review: Angiotensin-converting enzyme inhibitors and coronary heart disease prevention

Donnelly

Manning

2007

J Renin Angiotensin Aldosterone Syst

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A number of large randomised controlled trials have shown that angiotensin-converting enzyme (ACE) inhibitors, compared with placebo or other blood pressure-lowering drugs, improve coronary heart disease outcomes (fatal and nonfatal myocardial infarction, and coronary revascularisation) in diverse patient groups, e.g. in primary and secondary prevention, those with and without left ventricular dysfunction, and among hypertensive and non-hypertensive

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Section: Baselinementioning

confidence: 99%

Review: Angiotensin-converting enzyme inhibitors and coronary heart disease prevention

Donnelly

Manning

2007

J Renin Angiotensin Aldosterone Syst

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“…However, several studies have demonstrated an alteration in flow-mediated vasodilatation of large epicardial coronary arteries in hypertensive patients. [7][8][9] The consequences of hypertension on the endothelium are not limited to changes in the endothelial regulation of vasomotor function. In particular, it is now well known that the endothelium may possess potent anti-inflammatory properties.…”

Section: Hypertension and Endothelial Functionmentioning

confidence: 99%

“…Indeed, in essential hypertension, ACE inhibitors and angiotensin II type I receptor (AT 1 ) blockers improve the basal release of NO and the coronary or forearm blood flow responses to acetylcholine, 7,9,29,30 while ACE inhibitors or the perindopril-indapamide combination also improve flowmediated vasodilatation of brachial arteries.…”

Section: Renin-angiotensin System Blockersmentioning

confidence: 99%

Targeting endothelial dysfunction in hypertensive subjects

Thuillez

Richard

2005

J Hum Hypertens

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The endothelium is a favourite early target of cardiovascular risk factors and cardiovascular diseases like hypertension. This key role of the endothelium results from its capacity to respond to numerous autocrine and paracrine stimuli and to mechanical factors like shear stress but also from the pathophysiological consequences of endothelial dysfunction on vasomotor tone, arterial stiffness, arterial remodelling, and inflammation, all of which are factors that play a critical role in atherosclerosis and target-organ damage. In hypertension, endothelial dysfunction has been shown at the level of both resistance and conduit arteries and mainly results from an increase in nitric oxide (NO) degradation by interaction between NO and superoxide anions, while in experimental models of hypertension a decrease in NO production can also be observed. The fact that forearm endothelial dysfunction is a marker of future cardiovascular events in patients with hypertension stresses the importance of the clinical evaluation of endothelial function and of the evaluation of the effects of the different antihypertensive drug classes on this parameter. In this context, many studies have demonstrated that angiotensin-converting enzyme inhibitors, the perindopril-indapamide combination, and angiotensin II type I receptor (AT 1 ) blockers improve endothelium-dependent vasodilatation partly independently of arterial pressure. Both their antioxidant effects and the stimulation of the release of NO are involved in their beneficial effects. For calcium antagonists, only the recent drugs have been shown to improve endothelial function with a simultaneous improvement in several markers of oxidative stress. Finally, b-blockers classically do not affect endothelial function. Only nebivolol, a b-blocker with NO donor properties, has been shown to improve endothelial function, but this effect results from the increase in NO and not from the b-blocking properties of the drug.

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“…9,17 The cold pressor test provokes an adrenergic sympathetic reflex. 18 The increase in myocardial metabolic demand has been shown to cause an increase in coronary blood flow and, therefore, the flow-mediated dilation in epicardial coronary arteries.…”

Section: Response Of the Coronary Arteries To Cold Pressor Test In Hymentioning

confidence: 99%

“…17 Ghiadoni et al demonstrated that the angiotensin II type 1 receptor blocker candesartan enhanced the response of forearm blood flow to acetylcholine in hypertensive patients, indicating the attenuation of endothelial dysfunction in peripheral vasculature. 14 A recent study showed that acetylcholine-induced, endothelium-dependent relaxation in small resistance arteries in hypertensive patients was normalized by losartan.…”

Section: Effects Of Losartan On Response Of the Coronary Arteries To mentioning

confidence: 99%

Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension

Deng

Yang

et al. 2002

Clinical Cardiology

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SummaryBackground: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype.Hypothesis: The study sought to determine whether treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery (LMCA) by cold pressor test in patients with essential hypertension, as shown by echocardiography.Methods: The study population included 30 patients with mild to moderate essential hypertension and 30 matched healthy subjects. Measurements of the cold pressor test-induced and nitroglycerin-induced changes in LMCA diameter by echocardiography were performed at the end of the washout period and after 12 weeks of losartan administration.Results: The percent change in LMCA diameter induced by the cold pressor test in hypertensive patients (Ϫ3.5 ± 8.8%) was significantly lower than that in control subjects (10.2 ± 3.7%, p < 0.0001). After losartan treatment, the percent change (13.9 ± 8.4%) was significantly higher than that before losartan treatment (Ϫ3.5 ± 8.8%, p < 0.0001), but not significantly different between the 17 hypertensive patients with satisfactory control of blood pressure (13.8 ± 9.1%) and the 13 hypertensive patients without satisfactory control of blood

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Angiotensin-Converting Enzyme Inhibition Restores Flow-Dependent and Cold Pressor Test–Induced Dilations in Coronary Arteries of Hypertensive Patients

Abstract: ACE inhibition restored CPT-induced and flow-mediated coronary artery dilations in patients with essential hypertension. These results indicate that impaired coronary vasomotor responses may be reversible in recently diagnosed hypertension.

Cited by 116 publications

References 58 publications

Review: Angiotensin-converting enzyme inhibitors and coronary heart disease prevention

Review: Angiotensin-converting enzyme inhibitors and coronary heart disease prevention

Targeting endothelial dysfunction in hypertensive subjects

Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension

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