scholarly journals AT1 Receptor Gene Polymorphisms in relation to Postprandial Lipemia

2012 ◽  
Vol 2012 ◽  
pp. 1-6
Author(s):  
B. Klop ◽  
T. M. van den Berg ◽  
A. P. Rietveld ◽  
J. Chaves ◽  
J. T. Real ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gene Polymorphisms ◽  
Receptor Gene ◽  
Postprandial Lipemia ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Common ◽  
Receptor Gene Polymorphisms

Background. Recent data suggest that the renin-angiotensin system may be involved in triglyceride (TG) metabolism. We explored the effect of the common A1166C and C573T polymorphisms of the angiotensin II type 1 receptor (AT1R) gene on postprandial lipemia.Methods. Eighty-two subjects measured daytime capillary TG, and postprandial lipemia was estimated as incremental area under the TG curve. The C573T and A1166C polymorphisms of the AT1R gene were determined.Results. Postprandial lipemia was significantly higher in homozygous carriers of the 1166-C allele (9.39±8.36 mM*h/L) compared to homozygous carriers of the 1166-A allele (2.02±6.20 mM*h/L) (P<0.05). Postprandial lipemia was similar for the different C573T polymorphisms.Conclusion. The 1166-C allele of the AT1R gene seems to be associated with increased postprandial lipemia. These data confirm the earlier described relationships between the renin-angiotensin axis and triglyceride metabolism.

scholarly journals Association of angiotensin II type 1-receptor gene polymorphisms with the risk of developing hypertension in Mexican individuals

2011 ◽  
Vol 13 (1) ◽  
pp. 133-140 ◽  
Author(s):  
Nancy Martínez-Rodríguez ◽  
Carlos Posadas-Romero ◽  
Guillermo Cardoso ◽  
José Manuel Pérez-Rodríguez ◽  
Nonanzit Pérez-Hernández ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gene Polymorphisms ◽  
Complex Disease ◽  
Receptor Gene ◽  
Renin Angiotensin System ◽  
Similar Distribution ◽  
Increased Risk ◽  
Receptor Gene Polymorphisms ◽  
Genetic And Environmental Factors

Introduction: Hypertension is a complex disease in which a significant interaction between genetic and environmental factors takes place. The renin–angiotensin system plays an important role regulating blood pressure to maintain homeostasis and vascular tone. In the present work, the role of angiotensin II type 1-receptor (AGTR1) gene polymorphisms as susceptibility markers for hypertension was evaluated. Materials and methods: Five polymorphisms in the AGTR1 gene were genotyped by 5′ exonuclease TaqMan genotyping assays in 239 hypertensive and 371 non-hypertensive individuals. Results: A similar distribution of rs275651, rs275652, rs275653, and rs5183 polymorphisms was observed in both studied groups. Different distribution of rs5182 genotypes was observed between the studied groups ( p = 0.016). According to the co-dominant model, individuals with rs5182 CC genotype have a 1.83-fold increased risk of developing hypertension ( p = 0.009). Polymorphisms were distributed in two blocks: block 1 included the rs275651, rs275652, and rs275653 polymorphisms, whereas block 2 included the rs5183 and rs5182 polymorphisms. Individuals with hypertension showed increased frequency of ‘ CA’ haplotype of block 2 when compared to non-hypertensive individuals ( p = 0.015, odds ratio = 1.33). Conclusion: The results suggest that the rs5182 gene polymorphism could be involved in the risk of developing hypertension in Mexican individuals.

scholarly journals Angiotensin II Type 1 Receptor Gene Polymorphisms in Patients with Cardiac Hypertrophy.

1998 ◽  
Vol 39 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Alisher ISHANOV ◽  
Hiroshi OKAMOTO ◽  
Masashi WATANABE ◽  
Keiji YONEYA ◽  
Izumi NAKAGAWA ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Gene Polymorphisms ◽  
Receptor Gene ◽  
Receptor Gene Polymorphisms

scholarly journals Renin-Angiotensin System Blockers and the COVID-19 Pandemic

Hypertension ◽  
2020 ◽  
Vol 75 (6) ◽  
pp. 1382-1385 ◽  
Author(s):  
A.H. Jan Danser ◽  
Murray Epstein ◽  
Daniel Batlle
Keyword(s):  
Angiotensin Ii ◽  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Receptor Blockers ◽  
Renin Angiotensin System Blockers

During the spread of the severe acute respiratory syndrome coronavirus-2, some reports of data still emerging and in need of full analysis indicate that certain groups of patients are at risk of COVID-19. This includes patients with hypertension, heart disease, diabetes mellitus, and clearly the elderly. Many of those patients are treated with renin-angiotensin system blockers. Because the ACE2 (angiotensin-converting enzyme 2) protein is the receptor that facilitates coronavirus entry into cells, the notion has been popularized that treatment with renin-angiotensin system blockers might increase the risk of developing a severe and fatal severe acute respiratory syndrome coronavirus-2 infection. The present article discusses this concept. ACE2 in its full-length form is a membrane-bound enzyme, whereas its shorter (soluble) form circulates in blood at very low levels. As a mono-carboxypeptidase, ACE2 contributes to the degradation of several substrates including angiotensins I and II. ACE (angiotensin-converting enzyme) inhibitors do not inhibit ACE2 because ACE and ACE2 are different enzymes. Although angiotensin II type 1 receptor blockers have been shown to upregulate ACE2 in experimental animals, the evidence is not always consistent and differs among the diverse angiotensin II type 1 receptor blockers and differing organs. Moreover, there are no data to support the notion that ACE inhibitor or angiotensin II type 1 receptor blocker administration facilitates coronavirus entry by increasing ACE2 expression in either animals or humans. Indeed, animal data support elevated ACE2 expression as conferring potential protective pulmonary and cardiovascular effects. In summary, based on the currently available evidence, treatment with renin-angiotensin system blockers should not be discontinued because of concerns with coronavirus infection.

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