scholarly journals Angiotensin II formation from angiotensin converting enzyme and chymase-like enzyme in the normal human heart and in hearts from various mammals

1996 ◽  
Vol 27 (2) ◽  
pp. 156
Author(s):  
Eduardo Balcells ◽  
Qing C. Meng ◽  
Suzanne Oparil ◽  
Louis J. Dell'Italia
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Human Heart ◽  
Converting Enzyme ◽  
Normal Human

scholarly journals Expression of angiotensin-converting enzyme (CD143) identifies and regulates primitive hemangioblasts derived from human pluripotent stem cells

Blood ◽  
2008 ◽  
Vol 112 (9) ◽  
pp. 3601-3614 ◽  
Author(s):  
Elias T. Zambidis ◽  
Tea Soon Park ◽  
Wayne Yu ◽  
Ada Tam ◽  
Michal Levine ◽  
...  
Keyword(s):  
Stem Cells ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Embryoid Body ◽  
Embryonic Stem ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Embryonic Tissues ◽  
Angiotensin Ii Signaling ◽  
Normal Human

We report that angiotensin-converting enzyme (ACE), a critical physiologic regulator of blood pressure, angiogenesis, and inflammation, is a novel marker for identifying hemangioblasts differentiating from human embryonic stem cells (hESC). We demonstrate that ACE+CD45−CD34+/− hemangioblasts are common yolk sac (YS)–like progenitors for not only endothelium but also both primitive and definitive human lymphohematopoietic cells. Thrombopoietin and basic fibroblast growth factor are identified as critical factors for the proliferation of human hemangioblasts. The developmental sequence of human embryoid body hematopoiesis is remarkably congruent to the timeline of normal human YS development, which occurs during weeks 2 to 6 of human gestation. Furthermore, ACE and the renin-angiotensin system (RAS) directly regulate hemangioblast expansion and differentiation via signaling through the angiotensin II receptors AGTR1 and AGTR2. ACE enzymatic activity is required for hemangioblast expansion, and differentiation toward either endothelium or multipotent hematopoietic progenitors is dramatically augmented after manipulation of angiotensin II signaling with either AGTR1- or AGTR2-specific inhibitors. The RAS can therefore be exploited to direct the hematopoietic or endothelial fate of hESC-derived hemangioblasts, thus providing novel opportunities for human tissue engineering. Moreover, the initial events of human hematoendotheliogenesis can be delineated in a manner previously impossible because of inaccessibility to early human embryonic tissues.

scholarly journals 757-2 Angiotensin II Formation in the Intact Human Heart: Predominance of the Angiotensin Converting Enzyme Pathway

1995 ◽  
Vol 25 (2) ◽  
pp. 234A-235A
Author(s):  
Lawrence S. Zisman ◽  
William T. Abraham ◽  
Glenn E. Meixell ◽  
Brian N. Vamvakias ◽  
Brian D. Lowes ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Human Heart ◽  
Converting Enzyme

scholarly journals Angiotensin II formation in the intact human heart. Predominance of the angiotensin-converting enzyme pathway.

1995 ◽  
Vol 96 (3) ◽  
pp. 1490-1498 ◽  
Author(s):  
L S Zisman ◽  
W T Abraham ◽  
G E Meixell ◽  
B N Vamvakias ◽  
R A Quaife ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Human Heart ◽  
Converting Enzyme

Vascular Angiotensin-Converting Enzyme Expression Regulates Local Angiotensin II

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Dominik N. Müller ◽  
Jürgen Bohlender ◽  
Karl F. Hilgers ◽  
Duska Dragun ◽  
Olivier Costerousse ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Enzyme Expression

Comparative effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on pulmonary function in hypertensive patients

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Azza S. Jabbar ◽  
Nadheera F. Neamah ◽  
Ahmed H. Al-Darraji
Keyword(s):  
Angiotensin Ii ◽  
Adverse Effects ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Angiotensin Ii Receptor ◽  
Converting Enzyme Inhibitors ◽  
Hypertensive Patients ◽  
Receptor Blockers

Abstract Objectives Hypertension is a very common cardiovascular disease. Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) are widely used to treat hypertension. Many patients with hypertension are vulnerable to the antihypertensive adverse effects, which potentially reduces the adherence rate. Therefore, we conducted this study in order to evaluate the safety profile of both classes (ACEi and ARBs) on respiratory functions. Methods Two main groups of subjects were studied: first group is healthy control subjects and the second group is hypertensive patients, which was subdivided into subgroups in order to investigate the effect of all tested medications (captopril, enalapril, lisinopril, losartan, and valsartan). Respiratory efficiency was evaluated by measuring pulmonary function tests: FEV1, FVC, and FEV1%. Measurements were done using micromedical spirometer. Results We found that ARBs do not impair normal respiratory functions as measured by FEV1, FEV1%, and FVC in hypertensive patients. While ACEi treatments significantly reduced FEV1, FEV1%, and FVC compared to the other groups. Conclusions ARBs are not associated with any harmful effects on respiratory functions in hypertensive patients, unlike ACEi. As such, they could represent a first-choice treatment for hypertensive patients who are at high risk to the respiratory adverse effects.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

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