Assessment of the acute arterial effects of converting enzyme inhibition in essential hypertension: a double-blind, comparative and crossover study

Topouchian, Jirar; Brisac, Anne-Marie; Pannier, B.; Vicaut, Éric; Safar, Michel E.; Asmar, Roland

doi:10.1038/sj.jhh.1000581

Cited by 42 publications

(22 citation statements)

References 20 publications

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“…15,16 Although we did not measure pulse-wave velocity in our study, we speculate that quinapril may have favourably affected the timing of wave reflection as well (due to a decrease in arterial stiffness), because (i) quinapril increased both Dt and PP amplification (though nonsignificantly, since our sample size was not powered to detect a significant change of these parameters) and (ii) quinapril improved brachial artery responses (FMD) mediated by NO, which is an important determinant of arterial stiffness. 37 This is in line with evidence showing that quinapril reduces predominantly the stiffness of musculartype arteries, 44 such as the brachial artery and abdominal aorta.…”

Section: Central Haemodynamicssupporting

confidence: 77%

Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients

et al. 2007

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Section: Central Haemodynamicssupporting

confidence: 77%

Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients

et al. 2007

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“…There has been a recent surge in interest in drugs that not only reduce blood pressure but also modify the blood pressure curve. In this setting, nitrates, 27 calcium-channel blockers, 15 vasodilating beta-blockers 10 and ACE inhibitors [12][13][14] have all been shown to decrease AWR in the ascending aorta. This is in contrast to drugs that have no effect on AWR and arterial stiffness despite the same extent of blood pressure reduction.…”

Section: Valsartan-induced Effects On Arterial Wave Reflectionmentioning

confidence: 99%

“…27 In genetically hypertensive rats that have equal central and peripheral pressures, giving ACE inhibitors or calcium-channel blockers restores the pulse pressure gradient but hydralazine does not. 18 However, there is evidence that ACE inhibitors, by causing an equal decrease in brachial and aortic PP may not actually increase PP amplification, despite reducing wave reflection in patients with essential hypertension 14 although some studies have shown a restoration of pulse pressure gradient in patients with end-stage renal disease. 13 In the present study, we have observed that valsartan when added to an ACE inhibitor, preferentially decreased central pulse pressure, favourably modifying pulse pressure amplification, restoring it to normal values.…”

Section: Pulse Pressure Amplificationmentioning

confidence: 99%

“…9 Early wave reflection certainly has adverse haemodynamic consequences and delaying it would be logical therapy in the management of hypertension and left ventricular hypertrophy. [10][11][12][13][14][15] Attention is being directed at drugs that reduce early AWR and arterial stiffness, as not all antihypertensives have a beneficial effect on arterial stiffness and AWR despite the same level of blood pressure reduction. 16,17 Angiotensin-converting enzyme (ACE) inhibitors, in particular, have been shown to delay AWR and increase the pulse pressure gradient between the central and peripheral circulation in both animal 18 and human studies.…”

Section: Introductionmentioning

confidence: 99%

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Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Mahmud

Feely

2000

J Hum Hypertens

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Objective: Angiotensin-converting enzyme (ACE) inhibitors have beneficial effects on arterial compliance and distensibility and favourably modify the arterial pressure waveform in hypertensive patients. The objective of our study was to explore the possible effects of adding an ATII AT 1 receptor antagonist to an ACE inhibitor on augmentation pressure, a measure of arterial stiffness, and pulse pressure amplification in patients with poorly controlled essential hypertension. Design and methods: We studied a group of 18 patients with poorly controlled hypertension, despite at least three antihypertensive drugs including an ACE inhibitor, before, at 2 h and 2 weeks following the administration of 80 mg of valsartan, an ATII AT 1 receptor antagonist. Haemodynamic responses were measured by cuff sphygmomanometry, arterial pulse-wave analysis and the pulse pressure gradient was calculated as the difference between the brachial pulse pressure (cuff sphygmomanometry) and derived aortic pulse pressure (arterial pulse wave analysis). Results: Blood pressure decreased significantly (P Ͻ 0.001) and the effect was more pronounced on central

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“…Subsequently, Topouchian 44 showed that the acute administration of quinapril increased carotid artery distensibility and decreased PWV and wave reflections, an effect that was in part independent of BP reduction. A number of other studies have confirmed that other ACE-Is similarly reduce arterial stiffness (see Table 3).…”

Section: Ace Inhibitorsmentioning

confidence: 99%

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Mahmud

Feely

2004

J Renin Angiotensin Aldosterone Syst

114

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Arterial stiffness has recently been recognised as an independent risk factor for cardiovascular morbidity and mortality in hypertension. Many of the complications seen with angiotensin II (Ang II) excess or hyperaldosteronism -an increased event rate, left ventricular hypertrophy, endothelial dysfunction and target organ damage -are also associated with arterial stiffness. It is possible that reduced arterial compliance may be one mechanism whereby increased activity of the renin-angiotensin-aldosterone system (RAAS) produces adverse vascular effects. Common pathophysiological processes, altered collagen turnover and increased fibrosis may underlie both arterial stiffness and RAAS-associated vascular damage.While it is recognised that patients with hyperaldosteronism have increased arterial stiffness, the role of the RAAS in modulating arterial compliance in essential hypertension and in normotensive subjects is less clear cut. There is, however, more consistent data which show that drugs that interfere with Ang II or aldosterone, namely angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists, all reduce arterial stiffness. In many cases, this is to a greater extent than predicted from the extent of reduction in blood pressure (BP), suggesting a role for RAAS in vascular stiffness in hypertensive subjects. There is also evidence that combined ACE inhibitors (ACE-Is) and ARBs may have an additive effect in reducing stiffness. The reduction in cardiovascular mortality in end-stage renal disease patients treated with ACE-Is was preferentially seen in those who had reduced arterial stiffness. These data suggest that, in addition to regulation of vascular biology and BP, the RAAS is an important determinant of arterial stiffness in health and, more particularly, in disease. IntroductionThe pulse has retained a central role throughout the history of medicine. It was, however, more an art than a science until the 19th century, when sphygmography provided the first graphic recordings of the arterial pressure pulse. Abnormalities in the pulse wave contour were considered indicative of stiff arteries and subsequently used to diagnose hypertension and Bright's disease.About the same time as Tigerstedt and Bergman discovered renin, sphygmography was abandoned in favour of cuff sphygmomanometry. There has been a recent awakening in the field of arterial stiffness follow-

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Assessment of the acute arterial effects of converting enzyme inhibition in essential hypertension: a double-blind, comparative and crossover study

Cited by 42 publications

References 20 publications

Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients

Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients

Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

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