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1

Gene polymorphisms of the renin-angiotensin-aldosterone system and essential arterial hypertension in childhood

100%
Petrovic D., Bidivec M., Peterlin B.
Folia Biologica
|
2002
|
vol. 50
|
issue 1-2
53-56
EN
In order to investigate the contribution of candidate genes in the renin-angiotensin- -aldosterone system (RAAS) in pathogenesis of essential arterial hypertension (EAH), the I/D polymorphism of ACE gene, the M235T polymorphism of the angiotensinogen gene, and the angiotensin II type 1 receptor (AGT1R) A1166C gene polymorphism in a group of children with EAH were analyzed. Fifty-seven children, aged 8-19 years, with the diagnosis of EAH were included in the association study and were compared with 57 subjects with normal blood pressure (the control group). Arterial hypertension was defined as systolic/diastolic blood pressure measurements higher than 95 age-gender-height percentile of the adopted reference values. A trend was found towards an association between the M235T angiotensinogen gene polymorphism and EAH in childhood in a dominant model (odds ratio (OR) 2.1; 95 % confidence interval (CI) 0.9-5.1; P=0.077), whereas the authors failed to demonstrate an association between the ACE I/D gene polymorphism, or the A1166C AGT1R gene polymorphism and EAH in childhood. Additionally, evidence was found of interaction between the angiotensinogen-TT genotype and obesity on the risk of EAH in childhood (OR 19.3; 95% CI 1.1-77.3; P=0.014). In conclusion, the M235T angiotensinogen gene polymorphism is considered alone as well as in interaction with obesity to be risk factors for EAH in childhood.
2

Genetic polymorphism in rennin - angiotensin system and its association cardiovascular diseases

86%
Stajszczak M., Gminski J.
Postępy Higieny i Medycyny Doświadczalnej
|
1997
|
vol. 51
|
issue 1
171-183
EN
Myocardial infarction and stroke are the major cause of death in developed countries and are the clinical manifestation of atherosclerosis and hypertension. Both the environmental factors and genetic predisposition have an influence on the pathogenesis of these diseases. Despite we know lots of environmental risk factors and we made important advances in the prevention and treatment of mentioned diseases, our knowledge about the pathogenic linkage between genetic predisposition and cardiovascular diseases is still very little. Activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of hypertension and atherosclerosis. In spite of vasoconstrictor activity, angiotensin II can stimulate migration and proliferation of vascular smooth muscle cells, macrophage-foam cells formation, adhesion and agregation of platelets and fibrinolytic system inhibition. Angiotensin convertin enzyme inhibitors reduce the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. Blockade of renin-angiotensin system seems to be also effective in secondary prevention of myocardial infarction in men. In sum, the genetic variations inside the renin-angiotensin system which may affect the function of its components might have an influence on genetic predisposition to cardiovascular diseases. The paper deals with the current state of knowledge on association between polymorphic variations in renin gene, angiotensinogen gene, angiotensin converting enzyme gene and AT1 receptor gene and primary hypertension, ischeamic heart disease and myocardial infarction.
3

ACE-inhibitors and atherosclreosis

58%
Gminski J., Stajszczyk M.
Postępy Higieny i Medycyny Doświadczalnej
|
1996
|
vol. 50
|
issue 2
157-171
EN
The activation of the renin-angiotensin system has been proposed as a very important step in the pathogenesis of atherosclerosis. Accordingly, ACE-inhibitors and angiotensin II receptors antagonists showed their ability to reduce the atherosclerotic process in animals. Inhibition of renin-angiotensin system reduces the development of atherosclerotic lesion either in cholesterol-fed animals and in animals after vascular injury. The precise mechanism for this action may depend on the inhibition of other than hypertensive property of angiotensin II.
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