In vitro release of angiotensin-converting enzyme inhibitors, peroxyl-radical scavengers and antibacterial compounds by enzymatic hydrolysis of glycated gluten

2007 ◽  
Vol 45 (3) ◽  
pp. 327-334 ◽  
Author(s):  
María D. del Castillo ◽  
Antonella Ferrigno ◽  
Iolanda Acampa ◽  
Rosa C. Borrelli ◽  
Agustín Olano ◽  
...  
Keyword(s):  
Enzyme Inhibitors ◽  
Peroxyl Radical ◽  
In Vitro Release ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Radical Scavengers ◽  
Converting Enzyme Inhibitors ◽  
Antibacterial Compounds ◽  
Hydrolysis Of ◽  
Vitro Release

scholarly journals Suppression of Aldosterone Synthesis and Secretion by Channel Antagonists

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Keiichi Ikeda ◽  
Tsuyoshi Isaka ◽  
Kouki Fujioka ◽  
Yoshinobu Manome ◽  
Katsuyoshi Tojo
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitors ◽  
Renin Angiotensin System ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Channel Blockers ◽  
Converting Enzyme Inhibitors ◽  
Renin Angiotensin ◽  
Aldosterone Production ◽  
Ras Inhibitors

Aldosterone, a specific mineralocorticoid receptor (MR) agonist and a key player in the development of hypertension, is synthesized as a final product of renin-angiotensin-aldosterone system. Hypertension can be generally treated by negating the effects of angiotensin II through the use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin II type 1 receptor antagonists (ARBs). However, the efficacy of angiotensin II blockade by such drugs is sometimes diminished by the so-called “aldosterone breakthrough” effect, by which ACE-Is or ARBs (renin-angiotensin system (RAS) inhibitors) gradually lose their effectiveness against hypertension due to the overproduction of aldosterone, known as primary aldosteronism. Although MR antagonists are used to antagonize the effects of aldosterone, these drugs may, however, give rise to life-threatening adverse actions, such as hyperkalemia, particularly when used in conjunction with RAS inhibitors. Recently, several groups have reported that some dihydropyridine Ca2+channel blockers (CCBs) have inhibitory actions on aldosterone production inin vitroand in the clinical setting. Therefore, the use of such dihydropyridine CCBs to treat aldosterone-related hypertension may prove beneficial to circumvent such therapeutic problems. In this paper, we discuss the mechanism of action of CCBs on aldosterone production and clinical perspectives for CCB use to inhibit MR activity in hypertensive patients.

scholarly journals The Inhibition of Amylase and ACE Enzyme and the Reduction of Immunoreactivity of Sourdough Bread

Foods ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 656
Author(s):  
Anna Diowksz ◽  
Alicja Malik ◽  
Agnieszka Jaśniewska ◽  
Joanna Leszczyńska
Keyword(s):  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Wheat Bread ◽  
Converting Enzyme Inhibitors ◽  
Potential Health ◽  
Simulated Digestion ◽  
Sourdough Bread ◽  
Different Types ◽  
Amylase Inhibitors

This study examines the potential health benefits of different types of wheat sourdough bread against diseases of civilization. Celiac disease, diabetes and hypertension affect large numbers of the world’s population, increasing demand for novel treatments and ways of improving patient welfare. Different types of artisan breads were subjected to in vitro simulated digestion prior to analysis. The G12 test and ELISA with human sera were used for immunoreactivity analysis. The activity of α-amylase inhibitors and angiotensin-converting enzymes (ACE) was also assessed. The addition of sourdough to the analyzed wheat bread raised the content of α-amylase inhibitors and angiotensin-converting enzyme inhibitors while reducing their immunoreactivity. However, despite decreases in the antigenicity of the wheat flour proteins, the sera showed various reactions, depending on the individual patient’s susceptibility to gluten.

scholarly journals Angiotensin II effects on ischemic focal ventricular tachycardia are predominantly mediated through myocardial AT2 receptor

2009 ◽  
Vol 297 (5) ◽  
pp. H1889-H1898 ◽  
Author(s):  
Rakesh Gopinathannair ◽  
Ashok K. Chaudhary ◽  
Dezhi Xing ◽  
Debra Ely ◽  
Wei Zheng ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Angiotensin Ii ◽  
Enzyme Inhibitors ◽  
Three Dimensional ◽  
Coronary Artery Occlusion ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Artery Occlusion ◽  
Converting Enzyme Inhibitors ◽  
Triggered Activity

Ischemic focal ventricular tachycardia (VT) occurs in animals and humans. Angiotensin-converting enzyme inhibitors and receptor blockers reduce sudden death in patients with ischemic heart disease. In our dog model of coronary artery occlusion (CAO), we tested the hypothesis that angiotensin II (AGII) will selectively promote focal VT and that the specific AT2 blocker PD-123319 (PD), or AT1 blocker losartan, will affect this VT. Anesthetized dogs ( n = 90) underwent CAO, followed by three-dimensional activation mapping of inducible VT. Dogs without VT in 1–3 h after CAO received AGII, and those with VT received either PD or losartan. Focal endocardium excised from ischemic sites was studied in vitro with standard microelectrode. Of 33 dogs with no inducible VT, AGII infusion resulted in sustained VT of only focal Purkinje origin in 13 (39%) compared with 0 of 20 dogs with saline. Of 26 dogs with inducible VT at baseline, given PD, reinduction was blocked in 8 of 10 ( P < 0.05) focal VT, but only 1 of 15 with reentry. In contrast, of 11 dogs given losartan, reinduction of either mechanism was not blocked. In vitro triggered activity in Purkinje was blocked by PD in 13 of 19 ( P < 0.05), but not by losartan in 8. Also, triggered activity was promoted by AGII, losartan, or the combination in 9 of 12 tissues. AGII promotes only focal, mainly Purkinje ischemic VT. PD, but not losartan, preferentially blocked focal VT, which is likely due to triggered activity due to delayed afterdepolarizations in Purkinje.

Angiotensins and rheumatoid arthritis

2019 ◽  
Vol 56 (6) ◽  
pp. 753-759
Author(s):  
N. M. Savushkina ◽  
E. A. Galushko ◽  
N. V. Demidova ◽  
A. V. Gordeev
Keyword(s):  
Rheumatoid Arthritis ◽  
Enzyme Inhibitors ◽  
Renin Angiotensin System ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
The Body ◽  
Converting Enzyme Inhibitors ◽  
In Vivo Experiments ◽  
Endothelial Growth Factor

At present, the role of the renin-angiotensin system (RAS) in regulating the cardiovascular system and maintaining water and electrolyte homeostasis has been well studied. However, over the past decades, new components of the RAS have been identified, suggesting a wider range of its potential effects on the body. It is of fundamentally importance for rheumatologists to affect inflammation, including rheumatoid inflammation, through blockade of angiotensin (AT) II formation via the effects of AT 1–7 and angiotensin-converting enzyme inhibitors, as well as through suppression of angiogenesis, primarily by reducing the production of endothelial growth factor. The organ-protective and antiinflammatory potential of drugs that reduce the production of AT, which has been proven in in vitro and in vivo experiments, allows us to consider them as first-line angiotropic agents in patients with rheumatoid arthritis, especially in the presence of concomitant hypertension and/or nephropathy.

scholarly journals Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

2017 ◽  
Vol 18 (1) ◽  
pp. 147032031668719 ◽  
Author(s):  
Marzena Wojewodzka-Zelezniakowicz ◽  
Anna Gromotowicz-Poplawska ◽  
Wioleta Kisiel ◽  
Emilia Konarzewska ◽  
Janusz Szemraj ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Umbilical Vein ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Mrna Levels ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors

Introduction: The aim of this study was to investigate the effects of plasma and tissue angiotensin-converting enzyme inhibitors (ACE-Is) against propofol-induced endothelial dysfunction and to elucidate the involved mechanisms in vitro. Materials and methods: We examined the effects of propofol (50 μM), quinaprilat and enalaprilat (10−5 M) on fibrinolysis (t-PA, PAI-1, TAFI antigen levels), oxidative stress parameters (H2O2 and MDA antigen levels and SOD and NADPH oxidase mRNA levels) and nitric oxide bioavailability (NO2/NO3 concentration and NOS expression at the level of mRNA) in human umbilical vein endothelial cells (HUVECs). Results: We found that both ACE-Is promoted similar endothelial fibrinolytic properties and decreased oxidative stress in vitro. Propofol alone increased the release of antifibrinolytic and pro-oxidative factors from the endothelium and increased mRNA iNOS expression. We also found that the incubation of HUVECs in the presence of propofol following ACE-Is pre-incubation caused weakness of the antifibrinolytic and pro-oxidative potential of propofol and this effect was similar after both ACE-Is. Conclusions: This observation suggests that the studied ACE-Is exerted protective effects against endothelial cell dysfunction caused by propofol, independently of hemodynamics.

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