Design and Synthesis of Angiotensin Converting Enzyme (ACE) Inhibitors: Analysis of the Role of Tetrazole Ring Appended to Biphenyl Moiety

2022 ◽  
Vol 7 (2) ◽  
Author(s):  
Praveen K. Bayannavar ◽  
Ravindra R. Kamble ◽  
Shrinivas D. Joshi ◽  
Aravind R. Nesaragi ◽  
Saba Kauser J. Shaikh ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Tetrazole Ring ◽  
Converting Enzyme ◽  
Design And Synthesis

Endocrinologic Warfare: The Role of Angiotensin-Converting Enzyme Inhibitors in Congestive Heart Failure

1990 ◽  
Vol 3 (5) ◽  
pp. 318-331
Author(s):  
Mark A. Munger ◽  
Stephanie F. Gardner ◽  
Robert C. Jarvis
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Vasodilator Therapy ◽  
The Future

The angiotensin-converting enzyme (ACE) inhibitors represent the gold standard of vasodilator therapy for congestive heart failure through blunting of the endocrinologic manifestations of heart failure. The future role of these agents may be in the asymptomatic and mild stages of heart failure. ACE inhibitors have been shown to decrease morbidity and mortality with the natural history of this disease being altered. The future will bring many new ACE inhibitors to market, with the challenge for physicians and pharmacists to understand the important distinctions of each specific agent. © 1990 by W.B. Saunders Company.

Angiotensin-converting enzyme and the tumor microenvironment: mechanisms beyond angiogenesis

2013 ◽  
Vol 305 (3) ◽  
pp. R205-R215 ◽  
Author(s):  
Derick Okwan-Duodu ◽  
Jerome Landry ◽  
Xiao Z. Shen ◽  
Roberto Diaz
Keyword(s):  
Tumor Microenvironment ◽  
Substance P ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
T Regulatory Cells ◽  
Suppressor Cells ◽  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Converting Enzyme

The renin angiotensin system (RAS) is a network of enzymes and peptides that coalesce primarily on the angiotensin II type 1 receptor (AT1R) to induce cell proliferation, angiogenesis, fibrosis, and blood pressure control. Angiotensin-converting enzyme (ACE), the key peptidase of the RAS, is promiscuous in that it cleaves other substrates such as substance P and bradykinin. Accumulating evidence implicates ACE in the pathophysiology of carcinogenesis. While the role of ACE and its peptide network in modulating angiogenesis via the AT1R is well documented, its involvement in shaping other aspects of the tumor microenvironment remains largely unknown. Here, we review the role of ACE in modulating the immune compartment of the tumor microenvironment, which encompasses the immunosuppressive, cancer-promoting myeloid-derived suppressor cells, alternatively activated tumor-associated macrophages, and T regulatory cells. We also discuss the potential roles of peptides that accumulate in the setting of chronic ACE inhibitor use, such as bradykinin, substance P, and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), and how they may undercut the gains of anti-angiogenesis from ACE inhibition. These emerging mechanisms may harmonize the often-conflicting results on the role of ACE inhibitors and ACE polymorphisms in various cancers and call for further investigations into the potential benefit of ACE inhibitors in some neoplasms.

Current Perspective on the Use of Angiotensin-Converting Enzyme Inhibitors in the Management of Coronary (Atherosclerotic) Artery Disease

1997 ◽  
Vol 31 (12) ◽  
pp. 1499-1506 ◽  
Author(s):  
Judy WM Cheng ◽  
Mimi N Ngo
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
English Language ◽  
Data Extraction ◽  
Renin Angiotensin System ◽  
Therapeutic Monitoring ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Beneficial Effects

OBJECTIVE: To review the pathophysiology of atherosclerosis, the role of the renin—angiotensin system in atherogenesis, and studies supporting the potential beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in reducing cardiovascular events with long-term use. BACKGROUND: Through its action in converting angiotensin I to angiotensin II and by degrading bradykinin, local tissue ACE exerts many effects that can contribute to the development of atherosclerosis. Therefore, the use of ACE inhibitors can possibly result in antiatherogenic effects. Possible mechanisms for antiatherogenic effects of ACE inhibitors include: (1) reduction of blood pressure; (2) antiproliferative and antimigratory effects on vascular smooth muscle cells, neutrophils, and monocytes; (3) restoration of endothelial function; (4) stabilization of fatty plaque by preventing vasoconstriction; (5) antiplatelet effects; and (6) enhancement of endogenous fibrinolysis. DATA SOURCES: English-language clinical studies, abstracts, and review articles pertaining to the use of ACE inhibitors and atherosclerosis. STUDY SELECTION AND DATA EXTRACTION: Relevant human studies examining the role of ACE inhibitors and atherosclerosis. DATA SYNTHESIS: Studies evaluating the possible beneficial effects of ACE inhibitors in the development of atherosclerosis are reviewed and critiqued. Design of ongoing studies with clinical and surrogate end points are discussed. CONCLUSIONS: Based on current published studies, recommendations are made regarding the use of ACE inhibitors in atherosclerosis. Therapeutic monitoring parameters for efficacy and adverse effects are also reviewed.

scholarly journals The role of renin-angiotensin system and angiotensin-converting enzyme 2 (ACE2) in the development and course of viral infection COVID-19 in patients with diabetes mellitus

2020 ◽  
Vol 23 (3) ◽  
pp. 242-249
Author(s):  
O. K. Vikulova ◽  
Zamira Zuraeva ◽  
L. V. Nikankina ◽  
M. V. Shestakova
Keyword(s):  
Diabetes Mellitus ◽  
Angiotensin Converting Enzyme ◽  
Viral Infection ◽  
Ace Inhibitors ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin

The role of renin-angiotensin system (RAS) in general and angiotensin-converting enzyme 2 (ACE2) in particular in the pathogenesis and course of viral infection caused by SARS-CoV-2 (COVID-19) is of particular interest. This is due not only to the fact that ACE2 is a receptor for the virus the target cells. RAS hyperactivation in patients with arterial hypertension, cardiovascular disease and diabetes mellitus, is considered one of the most important factors for a more severe infection in persons with concomitant pathology. In addition, the effects of PAS blockage with angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) remains one of the most discussed topics in the literature on COVID-19. Thisreview presents the data on the interaction between the virus and the main components of RAS and the factors influencing their expression level, the impact of ACE inhibitors and ARBs therapy on the disease outcome, and presents theperspectives of the treatment with recombinant ACE 2.

scholarly journals A clinical dose of angiotensin-converting enzyme (ACE) inhibitor and heterozygous ACE deletion exacerbate Alzheimer's disease pathology in mice

2019 ◽  
Vol 294 (25) ◽  
pp. 9760-9770 ◽  
Author(s):  
Shuyu Liu ◽  
Fujiko Ando ◽  
Yu Fujita ◽  
Junjun Liu ◽  
Tomoji Maeda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Amyloid Precursor Protein ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Precursor Protein ◽  
Causative Role ◽  
Converting Enzyme ◽  
Clinical Dose

Inhibition of angiotensin-converting enzyme (ACE) is a strategy used worldwide for managing hypertension. In addition to converting angiotensin I to angiotensin II, ACE also converts neurotoxic β-amyloid protein 42 (Aβ42) to Aβ40. Because of its neurotoxicity, Aβ42 is believed to play a causative role in the development of Alzheimer's disease (AD), whereas Aβ40 has neuroprotective effects against Aβ42 aggregation and also against metal-induced oxidative damage. Whether ACE inhibition enhances Aβ42 aggregation or impairs human cognitive ability are very important issues for preventing AD onset and for optimal hypertension management. In an 8-year longitudinal study, we found here that the mean intelligence quotient of male, but not female, hypertensive patients taking ACE inhibitors declined more rapidly than that of others taking no ACE inhibitors. Moreover, the sera of all AD patients exhibited a decrease in Aβ42-to-Aβ40–converting activity compared with sera from age-matched healthy individuals. Using human amyloid precursor protein transgenic mice, we found that a clinical dose of an ACE inhibitor was sufficient to increase brain amyloid deposition. We also generated human amyloid precursor protein/ACE+/− mice and found that a decrease in ACE levels promoted Aβ42 deposition and increased the number of apoptotic neurons. These results suggest that inhibition of ACE activity is a risk factor for impaired human cognition and for triggering AD onset.

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