Plasma angiotensin-converting enzyme activity and carotid wall thickening.

Bonithon‐Kopp, Claire; Ducimetière, Pierre; Touboul, Pierre‐Jean; Fève, J M; Billaud, E; Courbon, Dominique; Heraud, V.

doi:10.1161/01.cir.89.3.952

Cited by 109 publications

(59 citation statements)

References 16 publications

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“…In this case the stent prevents the remodeling process, and restenosis is primarily a consequence of neointimal hyperplasia within the stent. 68 In accordance with this, a high expression of ACE was associated with a statistically significant increase in common carotid artery intima-media thickening, 69 and an association between DD genotype and the extent of common carotid artery intima-media thickening has been reported. 70 Those clinical data are concordant with our experimental results.…”

Section: Discussionsupporting

confidence: 58%

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Challah

Villard

Philippe

et al. 1998

ATVB

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Abstract-Two normotensive strains of rat, the Lou and Brown Norway (BN) strains, have contrasting levels of plasma angiotensin-converting enzyme (ACE). To investigate the degree of genetic determination of ACE expression, a polymorphic marker of the ACE gene was analyzed in inbred rats of the two strains. The two inbred strains were shown to bear different alleles for a polymorphic marker at the ACE gene. The segregation of the alleles of this marker and the plasma ACE levels were studied in a group of F2 rats issued from a cross between Lou and BN rats. The degree of genetic determination of plasma ACE activity was estimated to be 94% in the F2 cohort. The ACE locus accounts for 74% of total plasma ACE variance. ACE activity and mRNA expression in lungs were also genetically determined. The difference observed in ACE mRNA accumulation in the lungs between the two strains was due to a difference in the transcriptional rate of the ACE gene, as shown in nuclear run-on experiments. No differences were observed in arterial blood pressure of homozygous F2 progeny. In these animals, ACE genotype did not interfere with the pressor or the depressor responses to ACE-dependent vasoactive peptides. There was a significant effect of strain on constitutive or inducible membrane or soluble ACE activity in primary cultures of vascular cells. Neointima formation in the carotid artery 14 days after balloon injury was also influenced by the genotype in F2 homozygous progeny, whereas the medial area was not. These results demonstrate that there is a close relationship between the genetically determined ACE expression and the inducibility of the ACE gene. The degree of genetic determination of ACE expression in inbred rat strains offers a unique opportunity to study the interaction between genetic and environmental determinants of ACE expression and its involvement in response to experimental cardiovascular and renal injury. (Arterioscler Thromb Vasc Biol. 1998;18:235-243.)

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Section: Discussionsupporting

confidence: 58%

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Challah

Villard

Philippe

et al. 1998

ATVB

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“…4,38 In contrast, the data that support the contention that the D allele could also be a general marker of CVD are controversial. Positive studies [7][8][9][10][11][12][13][14] have in fact been contradicted not only by negative results basically for all types of CVD [15][16][17][18] (for reviews, see Koch et al 19 and Samani et al 45 ) but also by a study showing an association of the D allele with longevity in centenarians. 46 The mechanisms responsible for the supposed predisposition to developing CVD also remain largely speculative, because (1) the D/I polymorphism is located in intron 16 (ie, a noncoding region); (2) no change in the kinetic properties of ACE in relation with this polymorphism was documented 47 ; and (3) the contention that the higher ACE plasma levels associated with the D allele enhances Ang II generation in vivo 31 has been challenged.…”

Section: Discussionmentioning

confidence: 99%

“…5,6 The D allele has thereafter been associated with other CVD, including dilated and ischemic cardiomyopathy, coronary and carotid artery disease, coronary artery spasm, restenosis, left ventricular hypertrophy in hypertensives, left ventricular dysfunction, and, more recently, atherosclerotic renovascular hypertension. [7][8][9][10][11][12][13][14] However, opposite results for almost every clinical association have also been published, and therefore the value of the D/I genotyping for the purpose of cardiovascular risk stratification has been challenged [15][16][17][18][19][20][21][22][23] (for reviews, see Butler et al 24 and Agerholm-Larsen et al 25 ). Furthermore, the mechanisms by which the D allele would lead to a generalized increase in CVD risk remain largely speculative.…”

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confidence: 99%

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

et al. 2001

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Abstract-A deletion/insertion (D/I) polymorphism within the ACE gene may increase the risk of cardiovascular events through still unknown mechanisms. The latter may involve increased angiotensin II-induced NO breakdown and/or reduced agonist-mediated NO release. We therefore investigated whether the D allele of the ACE gene affects endothelium-dependent vasodilatation in mild-to-moderate primary hypertensive patients and healthy normotensive subjects. We compared in a cross-sectional study the forearm blood flow response of the 3 D/I genotypes with 5 incrementally increasing doses of the endothelium-dependent vasodilator acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1) in 142 subjects: 103 mild-to-moderate uncomplicated primary hypertensives (49.3Ϯ9.1 years old, 152Ϯ11/99Ϯ5 mm Hg) and 39 normotensives (44.6Ϯ15.3 years old, 122Ϯ12/78Ϯ6 mm Hg). We also assessed the endothelium-independent vasodilatation in the forearm, as blood flow response to 3 incrementally increasing doses of sodium nitroprusside (1, 2, and 4 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1 ). The overall genotype distribution was II, nϭ10; ID, nϭ70; and DD, nϭ62. It did not differ significantly between primary hypertensives and normotensives. A significant blunting of endothelium-dependent vasodilatation in primary hypertensive patients compared with normotensive subjects (PϽ0.001) was found. No effect of the DI genotype on endothelium-dependent and -independent vasodilatation was detected. Thus, these results obtained in a relatively large population do not support the contention that the D allele is associated with a blunting of either stimulated endothelial NO or donated NO responses in both mild-to-moderate primary hypertensive patients and normotensive subjects. (Hypertension. 2001;37:293-300.)

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“…A localized echostructure encroaching into the vessel lumen was considered to be a plaque if the CCA intima-media thickness was Ͼ50% thicker than at neighboring sites. 18 Cardiac measurements were performed in a blinded fashion by two physicians (G.M.L. and B. Pannier) according to the methods of the American Society of Echocardiography.…”

Section: Study Design and Arterial And Cardiac Measurementsmentioning

confidence: 99%

Influence of Biochemical Alterations on Arterial Stiffness in Patients With End-stage Renal Disease

Blacher

Demuth

Guérin

et al. 1998

ATVB

190

115

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Abstract-The incremental elastic modulus of the common carotid and radial arteries is increased in patients with end-stage renal disease (ESRD), independently of blood pressure, wall stress, and the presence of atherosclerotic alterations. Whether biochemical factors may be involved in the arterial changes and related to renal dysfunction remain largely ignored. To assess this question, we measured aortic (carotid-femoral), upper-limb (carotid-radial), and lower-limb (femoral-tibial) pulse wave velocity (PWV) in 74 ESRD patients undergoing hemodialysis in comparison with 57 control subjects similar in age, sex ratio, and mean blood pressure. We evaluated arterial blood presure by sphygmomanometry, aortic calcifications and cardiac mass by echography, and routine biochemical parameters, total plasma homocysteine, and plasma endothelin levels by standard techniques. In the population of patients with ESRD, on the basis of multiple stepwise regression analysis, aortic PWV was positively and independently correlated with systolic blood pressure (PϽ.0001), age (PϽ.0001), prevalence of aortic calcification (Pϭ.0004), and the prevalence of diabetes mellitus (Pϭ.0043). Upper-limb PWV was influenced exclusively by mean blood pressure (PϽ.0001). Lower-limb PWV was positively and independently correlated with plasma total homocysteine (Pϭ.0004) and plasma endothelin (Pϭ.0187) only. At any vascular site, PWV was not independently correlated with tobacco consumption; plasma levels of cholesterol, triglyceride, fibrinogen, or hemoglobin; body mass index; or the presence of bilateral nephrectomy. Finally, plasma homocysteine was independently correlated with cardiac mass (Pϭ.0022). This study provides evidence that in ESRD patients, the stiffness of the arterial wall and cardiac mass are strongly influenced by biochemical factors related to the kidney alterations and are independent of age and blood pressure level. Increased plasma endothelin and homocysteine may be specifically involved in the vascular damage of lower limbs. (Arterioscler Thromb Vasc Biol. 1998;18:535-541.)

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Plasma angiotensin-converting enzyme activity and carotid wall thickening.

Abstract: The results of the study suggest that chronic exposure to high levels of plasma ACE could be involved in structural changes of the arterial wall.

Cited by 109 publications

References 16 publications

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Influence of Biochemical Alterations on Arterial Stiffness in Patients With End-stage Renal Disease

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