Inhibition of converting enzyme prevents the age-related decline in endothelium-dependent hyperpolarization

Edhf 2000 ◽  
2003 ◽  
pp. 446-452
Keyword(s):  
Converting Enzyme ◽  
Age Related

scholarly journals Age-Related Differences in the Expression of Most Relevant Mediators of SARS-CoV-2 Infection in Human Respiratory and Gastrointestinal Tract

2021 ◽  
Vol 9 ◽  
Author(s):  
Roberto Berni Canani ◽  
Marika Comegna ◽  
Lorella Paparo ◽  
Gustavo Cernera ◽  
Cristina Bruno ◽  
...  
Keyword(s):  
Small Intestine ◽  
Angiotensin Converting Enzyme ◽  
Clinical Features ◽  
Clinical Severity ◽  
Nasal Epithelium ◽  
Pcr Analysis ◽  
Upper Respiratory Tract ◽  
Converting Enzyme ◽  
Age Related ◽  
Transmembrane Serine Protease

Background: Clinical features of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection seem to differ in children compared to that in adults. It has been hypothesized that the lower clinical severity in children could be influenced by differential expression of the main host functional receptor to SARS-CoV-2, the angiotensin-converting enzyme 2 (ACE2), but data are still conflicting. To explore the origin of age-dependent clinical features of coronavirus disease 2019 (COVID-19), we comparatively evaluated the expression in children and adult subjects of the most relevant mediators of the SARS-CoV-2 infection: ACE2, angiotensin-converting enzyme 1 (ACE1), transmembrane serine protease-2 (TMPRSS2), and neuropilin-1 (NRP1), at upper respiratory tract and small intestine level.Methods: The expression of ACE2, ACE1, TMPRSS2, and NRP1 in nasal epithelium and in small intestine epithelium was investigated by quantitative real-time PCR analysis.Results: We found no differences in ACE2, ACE1, and TMPRSS2 expression in the nasal epithelium comparing children and adult subjects. In contrast, nasal epithelium NRP1 expression was lower in children compared to that in adults. Intestinal ACE2 expression was higher in children compared to that in adults, whereas intestinal ACE1 expression was higher in adults. Intestinal TMPRSS2 and NRP1 expression was similar comparing children and adult subjects.Conclusions: The lower severity of SARS-CoV-2 infection observed in children may be due to a different expression of nasal NRP1, that promotes the virus interaction with ACE2. However, the common findings of intestinal symptoms in children could be due to a higher expression of ACE2 at this level. The insights from these data will be useful in determining the treatment policies and preventive measures for COVID-19.

Serum angiotensin-converting enzyme in healthy and sarcoidotic children: comparison with the reference interval for adults

1990 ◽  
Vol 36 (2) ◽  
pp. 344-346 ◽  
Author(s):  
B Bénéteau-Burnat ◽  
B Baudin ◽  
G Morgant ◽  
F C Baumann ◽  
J Giboudeau
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Hormonal Regulation ◽  
Reference Interval ◽  
Healthy Children ◽  
Age Group ◽  
Converting Enzyme ◽  
Serum Angiotensin Converting Enzyme ◽  
Age Related ◽  
Ace Activity ◽  
Physiological Variations

Abstract Angiotensin-converting enzyme (ACE) was measured in serum of 187 healthy children between the ages six months and 18 years. Results were pooled for five-year age intervals and compared with the reference values for adults that we previously determined [Clin Chem 1986;32:884-6). Results for each age group were also studied as a function of sex. Children had higher ACE activities in serum than did adults (P less than 0.001), but these activities were age-related only from age four to 18 years. Adolescents showed sex-related differences, with higher serum ACE activities in boys than in girls (P less than 0.05). Both sex- and age-related differences may be related to a steroid hormonal regulation of ACE biosynthesis. We also verified that children with sarcoidosis (n = 20) had significantly increased serum ACE activity. Such physiological variations in serum ACE activity must be taken into account for diagnosing sarcoidosis in children, for following the course of the disease, and for evaluating the accuracy of therapy.

scholarly journals Angiotensin-converting enzyme 2 deficiency accelerates and angiotensin 1-7 restores age-related muscle weakness in mice

2018 ◽  
Vol 9 (5) ◽  
pp. 975-986 ◽  
Author(s):  
Hikari Takeshita ◽  
Koichi Yamamoto ◽  
Satoko Nozato ◽  
Masao Takeda ◽  
So-ichiro Fukada ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Muscle Weakness ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Age Related

Effect of chronic ANG I-converting enzyme inhibition on aging processes. III. Endothelial function of mesenteric arterial bed of rat

1994 ◽  
Vol 267 (1) ◽  
pp. R136-R143
Author(s):  
J. Atkinson ◽  
R. Tatchum-Talom ◽  
B. Corman
Keyword(s):  
Enzyme Inhibitor ◽  
Muscarinic Agonist ◽  
Converting Enzyme ◽  
Hypotensive Action ◽  
Age Related ◽  
Mesenteric Arterial Bed ◽  
Converting Enzyme Inhibition ◽  
Old Rats ◽  
Arteriolar Tone

Age-related changes in endothelial (E) function were studied in mesenteric arterial bed (MAB) preparations removed from male, normotensive, WAG/Rij rats. At the age of 6 mo, one-half of the animals was assigned to chronic treatment with a hypotensive dose of an angiotensin I (ANG I)-converting enzyme inhibitor (ACEI; perindopril, 1 mg.kg-1.day-1 po). Animals were killed at 6, 12, 24, or 30 mo of age; the MAB was perfused in vitro, perfusion pressure (PP) being taken as an index of arteriolar tone. Disruption of E function produced a fall in baseline PP in all groups except 30-mo-old rats, suggesting that 1) baseline tone is maintained by the release of E vasoconstrictor factor(s) and 2) this mechanism is impaired in 30-mo-old rats. The muscarinic agonist, carbachol, antagonized vasoconstriction produced by norepinephrine (NE) in the presence of E. This mechanism was impaired in 30-mo-old rats. NE vasoconstriction increased following disruption of E, suggesting that NE release of endothelium-derived relaxing factor attenuates vasoconstriction. This mechanism was impaired in 30-mo-old rats. Chronic ACEI postponed the age-related decrease in E function, possibly due to a direct effect, or an indirect effect via the prolonged hypotensive action of such treatment.

scholarly journals Pharmacogenetic effects of angiotensin-converting enzyme inhibitors over age-related urea and creatinine variations in patients with dementia due to Alzheimer disease

2016 ◽  
pp. 76-80 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Juliana Marília Berretta ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Alzheimer Disease ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Blood Levels ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Age Related

Background: Renal function declines according to age and vascular risk factors, whereas few data are available regarding genetically-mediated effects of anti-hypertensives over renal function. Objective: To estimate urea and creatinine variations in dementia due to Alzheimer disease (AD) by way of a pharmacogenetic analysis of the anti-hypertensive effects of angiotensin-converting enzyme inhibitors (ACEis). Methods: Consecutive outpatients older than 60 years-old with AD and no history of kidney transplant or dialytic therapy were recruited for prospective correlations regarding variations in fasting blood levels of urea and creatinine in one year, considering ACE genotypes of rs1800764 and rs4291 and their respective haplotypes, and treatment with ACEis along with blood pressure variations. Results: For 190 patients, 152 had arterial hypertension, and 122 used ACEis. Minor allele frequencies were 0.492 for rs1800764-C and 0.337 for rs4291-T, both in Hardy-Weinberg equilibrium. There were no overall significant yearly variations in levels of urea and creatinine, but their concurrent variations were positively correlated (ρ <0.0001). Each A allele of rs4291 led to an yearly urea increase of 3.074 mg/dL, and an yearly creatinine increase of 0.044 mg/dL, while the use of ACEis was protective regarding creatinine variations. The use of ACEis was also protective for carriers of rs1800764-CT/rs4291-AA, while carriers of rs1800764-CT/rs4291-AT had steeper reductions in creatinine levels, particularly when they were treated with ACEis. Conclusions: Effects of ACEis over creatinine variations are genetically mediated and independent of blood pressure variations in older people with AD.

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