Serum angiotensin converting enzyme activity in pulmonary diseases: Correlation with lung function parameters

Uçar, Gülberk; Yıldırım, Zeki; Ataol, Ebru; Erdoğan, Yurdanur; Biber, Çiğdem

doi:10.1016/s0024-3205(97)00616-4

Cited by 22 publications

(10 citation statements)

References 13 publications

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“…The vascular risk factors that might be related to serum ACE activity are not well known. In one report, smoking and blood pressure 30 , and in another, male sex and history of hypertension 31 correlated with the serum ACE activity. In our sample, the I/D polymorphism and smoking together explained 28% of the variance in ACE activity.…”

Section: Discussionmentioning

confidence: 92%

A study of gene-environment interaction on the gene for angiotensin converting enzyme: a combined functional and population based approach

Sayed‐Tabatabaei

Schut²,

Hofman³

et al. 2004

Journal of Medical Genetics

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Introduction: Studies on the role of the insertion/deletion (I/D) polymorphism of the gene coding for angiotensin converting enzyme (ACE) in atherosclerosis have been inconsistent. In a meta-analysis, we recently showed that this relationship is stronger in high risk populations. In this paper, we used a combined functional and population based approach to investigate the gene-environment interaction of the ACE I/D polymorphism in relation to carotid artery wall thickness. Methods: The study was part of the Rotterdam Study, a prospective population based cohort study. In 5321 subjects, IMT was measured in the carotid arteries by ultrasonography and ACE genotype was determined by size analysis of polymerase chain reaction products. Results: In multiple regression analysis, I/D polymorphism and smoking were the main determinants for plasma ACE activity (r 2 = 0.28). There was a positive association between the D allele of the I/D polymorphism and carotid artery thickness among current smokers (p = 0.03). Subjects carrying only one of the risk factors (smoking or the D allele) did not show significant differences in IMT compared with the non-/former smokers group carrying two II alleles, while carriers of both risk factors had significant higher IMT. The association was not present in non-/former smokers. Discussion: The results provide further evidence that genetic and environmental factors interact in the formation of the arterial lesions. This study shows that large population based studies can be extremely helpful in unravelling the genetic origin of complex diseases such as atherosclerosis.

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Section: Discussionmentioning

confidence: 92%

A study of gene-environment interaction on the gene for angiotensin converting enzyme: a combined functional and population based approach

Sayed‐Tabatabaei

Schut²,

Hofman³

et al. 2004

Journal of Medical Genetics

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“…Increased ACE activity has been demonstrated in COPD patients [153,154]. A study found the ACE D/D genotype to be more prevalent in smokers that developed COPD and to signify a higher risk of a smoker developing chronic airflow obstruction, although serum levels of ACE were not measured [155].…”

Section: The Role Of Ace In Acute and Chronic Lung Diseasementioning

confidence: 99%

“…In a recent meta-analysis study that included 18 case-control studies, subgroup analysis by age and ethnicity showed children and Asians as the ones who are more susceptible, with a 59% greater risk for asthma [168]. Another study showed serum ACE levels to correlate negatively with oxygen tension and lung function parameters in patients with extrinsic but not intrinsic asthma, and emphysema [153].…”

Section: The Role Of Ace In Acute and Chronic Lung Diseasementioning

confidence: 99%

Local Renin-Angiotensin II Systems, Angiotensin-Converting Enzyme and its Homologue ACE2: Their Potential Role in the Pathogenesis of Chronic Obstructive Pulmonary Diseases, Pulmonary Hypertension and Acute Respiratory Distress Syndrome

Kaparianos¹,

Argyropoulou²

2011

CMC

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Renin-angiotensin II-aldosterone axis has long been known as a regulator of blood pressure and fluid homeostasis. Yet, local renin-angiotensin II systems have been discovered and novel actions of angiotensin II (AngII) have emerged among which its ability to act as a immunomodulator and profibrotic molecule. The enzyme responsible for its synthesis, Angiotensin-converting-enzyme (ACE), is present in high concentrations in lung tissue. In the present paper, we review data from studies of the past decade that implicate AngII and functional polymorphisms of the ACE gene that increase ACE activity with increased susceptibility for asthma and chronic obstructive pulmonary disease (COPD) and for pulmonary hypertension. Moreover, drugs that inhibit the synthesis of AngII (ACE inhibitors) or that antagonize its actions on its receptors (Angiotensin II receptor blockers -ARBs) have been shown to provide beneficial effects. Another recent discovery reviewed is the presence of a homologue of ACE, ACE2, which cleaves a single amino acid from AngII and forms a heptapeptide with vasodilatory actions, Ang 1-7. The balance between ACE and ACE2 is crucial for controlling AngII levels. ACE and ACE2 also appear to modify the severity of Acute Respiratory Distress Syndrome (ARDS), with ACE2 playing a protective role. Finally, mention is made to the recent discovery of ACE2 as a receptor for the SARS Corona Virus.

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“…ACE is primarily synthesized by vascular endothelial cell and is localized in the lung and kidney vasculature, brain, small intestine, and alveolar macrophages [27]. Alterations of serum ACE occur in certain diseases such as sarcoidosis, leprosy, silicosis and asbestosis, tuberculosis, asthma, and malignant disease [1,7,8,15,16,21,28,39]. ACE in peripheral blood is thought to be identical with the lung enzyme and is proportional to blood oxygen concentration, suggesting that serum ACE activity is in good correlation with the enzyme level of the pulmonary tissue [4].…”

Section: Introductionmentioning

confidence: 99%

Gene Polymorphisms of Endothelial Nitric Oxide Synthase and Angiotensin-converting Enzyme in Patients with Lung Cancer

Cheon

Choi

Lee

et al. 2000

Lung

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The objectives of this study were to examine the possible involvement of endothelial nitric oxide synthase (ecNOS) and angiotensin-converting enzyme (ACE) genes in the genetic basis of lung cancer. Two hundred eighteen patients with lung cancer and 121 healthy subjects were included in this study. The ecNOS and ACE genotypes were determined in all subjects by polymerase chain reaction. The distribution of genotypes of ecNOS gene was significantly different in the lung cancer group than in the control population. ACE genotype distribution was not significantly different in the lung cancer group compared with the control group. These results suggest that polymorphisms of the ecNOS gene, but not the ACE gene, may be associated with the development of lung cancer.

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Serum angiotensin converting enzyme activity in pulmonary diseases: Correlation with lung function parameters

Cited by 22 publications

References 13 publications

A study of gene-environment interaction on the gene for angiotensin converting enzyme: a combined functional and population based approach

A study of gene-environment interaction on the gene for angiotensin converting enzyme: a combined functional and population based approach

Local Renin-Angiotensin II Systems, Angiotensin-Converting Enzyme and its Homologue ACE2: Their Potential Role in the Pathogenesis of Chronic Obstructive Pulmonary Diseases, Pulmonary Hypertension and Acute Respiratory Distress Syndrome

Gene Polymorphisms of Endothelial Nitric Oxide Synthase and Angiotensin-converting Enzyme in Patients with Lung Cancer

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