scholarly journals Roles of the Two Active Sites of Somatic Angiotensin-Converting Enzyme in the Cleavage of Angiotensin I and Bradykinin

2003 ◽  
Vol 93 (2) ◽  
pp. 148-154 ◽  
Author(s):  
Dimitris Georgiadis ◽  
Fabrice Beau ◽  
Bertrand Czarny ◽  
Joël Cotton ◽  
Athanasios Yiotakis ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Active Sites ◽  
Converting Enzyme ◽  
Angiotensin I

scholarly journals Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19

2021 ◽  
Vol 4 (Special2) ◽  
pp. 389-394
Author(s):  
Angela Madalina Lazar
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Current Knowledge ◽  
Angiotensin Receptor Blockers ◽  
Protective Effects ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.

scholarly journals Angiotensin-Converting Enzyme C-Terminal Catalytic Domain Is the Main Site of Angiotensin I Cleavage In Vivo

Hypertension ◽  
2008 ◽  
Vol 51 (2) ◽  
pp. 267-274 ◽  
Author(s):  
Sebastien Fuchs ◽  
Hong D. Xiao ◽  
Christine Hubert ◽  
Annie Michaud ◽  
Duncan J. Campbell ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Catalytic Domain ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Main Site

scholarly journals Capillaries of the adrenal cortex possess aminopeptidase A and angiotensin-converting-enzyme activities

1980 ◽  
Vol 186 (2) ◽  
pp. 605-608 ◽  
Author(s):  
P J Del Vecchio ◽  
J W Ryan ◽  
A Chung ◽  
U S Ryan
Keyword(s):  
Adrenal Gland ◽  
Angiotensin Converting Enzyme ◽  
Adrenal Cortex ◽  
Enzyme Activities ◽  
Capillary Endothelium ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Aminopeptidase A

The enzymes required to convert the prohormone angiotensin I into angiotensins II and III, secretagogues of aldosterone, are enriched in association with capillary endothelium isolated from rat adrenal cortex. Thus the secretion of aldosterone may be controlled, in part, by processing of peptides occurring within the adrenal gland itself.

scholarly journals Selective Angiotensin-Converting Enzyme C-Domain Inhibition Is Sufficient to Prevent Angiotensin I–Induced Vasoconstriction

Hypertension ◽  
2005 ◽  
Vol 45 (1) ◽  
pp. 120-125 ◽  
Author(s):  
Joep H.M. van Esch ◽  
Beril Tom ◽  
Vincent Dive ◽  
Wendy W. Batenburg ◽  
Dimitris Georgiadis ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Angiotensin I

Regional Haemodynamic Effects of Captopril, Enalaprilat and Lisinopril in Conscious Water-Replete and Water-Deprived Brattleboro Rats

1990 ◽  
Vol 79 (4) ◽  
pp. 393-401 ◽  
Author(s):  
A. F. Muller ◽  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Effective Dose ◽  
Pressor Response ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Haemodynamic Effects ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Vascular Conductance ◽  
Converting Enzyme Inhibitors ◽  
Renal Flow

1. The regional haemodynamic effects of intravenous bolus doses of captopril, enalaprilat and lisinopril were assessed in conscious Brattleboro (i.e. vasopressin-deficient) rats, chronically instrumented with miniaturized pulsed Doppler probes and intravascular catheters. 2. Responses to incremental doses of each drug (spanning the median effective dose for the inhibition of the pressor response to angiotensin I) were examined in both water-replete and water-deprived states. 3. In the water-replete state, the haemodynamic profiles of captopril, enalaprilat and lisinopril were generally similar, with incremental doses causing rises in mesenteric and renal flow and, to a lesser extent, hindquarters flow. There were small tachycardias and only slight falls in mean blood pressure. 4. In the water-deprived state, the effects of all three drugs were greatly enhanced; tachycardic and hypotensive effects occurred together with increases in mesenteric, renal and hindquarters flows. However, for renal flow and renal vascular conductance the effectiveness of the drugs decreased in the order enalaprilat > captopril > lisinopril, whereas for mesenteric flow and mesenteric vascular conductance the order was captopril > enalaprilat > lisinopril. 5. Since marked haemodynamic actions were seen with doses one-tenth of the median effective dose for the inhibition of the pressor effect of angiotensin I, it is likely these effects were due to inhibition of angiotensin-converting enzyme, although not necessarily to inhibition of angiotensin II production. There were differences between the regional haemodynamic effects of the drugs at higher doses (10 × the median effective dose and 2 mg/kg), these differences supporting the proposition that in future it may be possible to design angiotensin-converting enzyme inhibitors with regionally selective haemodynamic effects.

scholarly journals Sustained Dysregulation of the Plasma Renin-angiotensin System in Acute COVID-19

2021 ◽  
Author(s):  
Kevin Burns ◽  
Matthew Cheng ◽  
Todd Lee ◽  
Allison McGeer ◽  
David Sweet ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Clinical Trial Registration ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

Abstract SARS-CoV-2 enters cells by binding to angiotensin-converting enzyme 2 (ACE2), and COVID-19 infection may therefore induce changes in the renin-angiotensin system (RAS). To determine the effects of COVID-19 on plasma RAS components, we measured plasma ACE, ACE2, and angiotensins I, (1-7), and II in 46 adults with COVID-19 at hospital admission and on days 2, 4, 7 and 14, compared to 50 blood donors (controls). We compared survivors vs. non-survivors, males vs. females, ventilated vs. not ventilated, and angiotensin receptor blocker (ARB) and angiotensin-converting enzyme (ACE) inhibitor-exposed vs. not exposed. At admission, COVID-19 patients had higher plasma levels of ACE (p=0.012), ACE2 (p=0.001) and angiotensin-(1-7) (p<0.001) than controls. Plasma ACE and ACE2 remained elevated for 14 days in COVID-19 patients, while plasma angiotensin-(1-7) decreased after 7 days. In adjusted analyses, plasma ACE was higher in males vs. females (p=0.042), and plasma angiotensin I was significantly lower in ventilated vs. non-ventilated patients (p=0.001). In summary, plasma ACE and ACE2 are increased for at least 14 days in patients with COVID-19 infection. Angiotensin-(1-7) levels are also elevated, but decline after 7 days. The results indicate dysregulation of the RAS with COVID-19, with increased circulating ACE2 throughout the course of infection.Clinical Trial Registration: https://clinicaltrials.gov/ Unique Identifier: NCT04510623

scholarly journals The Effect of Angiotensin-Converting Enzyme Gene Polymorphisms in the Coronary Slow Flow Phenomenon at South Sumatra, Indonesia Population

2020 ◽  
Vol 8 (A) ◽  
pp. 225-230
Author(s):  
Ali Ghanie ◽  
Radiyati Umi Partan ◽  
Taufik Indrajaya ◽  
Zulkhair Ali ◽  
Mgs Irsan Saleh ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Linked Immunosorbent Assay ◽  
Slow Flow ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Flow Phenomenon ◽  
Two Samples ◽  
Coronary Slow Flow ◽  
Coronary Slow Flow Phenomenon

BACKGROUND: The coronary slow flow phenomenon (CSFP) is believed to be affected by endothelial dysfunction ruled by renin, angiotensin, aldosterone, and the angiotensin-converting enzyme (ACE). The gene of ACE has been characterized in humans by a major insertion (I)/deletion (D) polymorphism. Serum ACE levels were associated with I/D polymorphism in the ACE-encoding gene. AIM: This study explored and analyzed the role of ACE gene polymorphism risk factors with the incidence of CSFP in the population of South Sumatra, Indonesia. METHODS: This study was a cross-sectional analytic observational study. A total of 112 CSFP and non- CSFP patients participated in this study. Blood was obtained from the study subjects then processed. Angiotensin I and aldosterone levels were examined using the enzyme-linked immunosorbent assay. The Judkins method was used in the assessment of coronary angiography, which was carried out through the femoral artery. For the examination of ACE I/D polymorphisms, genome deoxyribonucleic acid was extracted from blood cells (leukocytes), using the Wizard’s purification system and examined using the polymerase chain reaction method. All data were evaluated through the Chi-square test, two samples t-test, and Mann–Whitney U-test. All tests used two-sided significance and p < 0.05 was considered statistically significant. RESULTS: ACE I/D gene polymorphism possessed a significant effect in increasing the risk of CSFP. Genotype II polymorphism increased the risk of CSFP as much as 6.9 times compared to individuals with ID/DD genotype. The existence of allele I increased the risk of CSFP 5.7 times compared to allele D. Levels of angiotensin I and aldosterone were increased significantly in patients with CSFP. CONCLUSION: ACE I/D gene polymorphism possessed a significant effect in increasing the risk of CSFP. Genotype of II was the risk factor for the development of CSFP in population of South Sumatra, Indonesia.

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