Document Detail


Contribution of angiotensin I converting enzyme gene polymorphism and angiotensinogen gene polymorphism to blood pressure regulation in essential hypertension.
MedLine Citation:
PMID:  9524045     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The renin-angiotensin system (RAS) is involved in the pathogenesis of essential hypertension. In the present study we examined the genotype frequencies of the insertion/deletion polymorphisms of the ACE gene and the M235T polymorphism of the Angiotensinogen (Agt) gene in patients with essential hypertension in comparison with normotensive subjects. In hypertensive patients functional effects of blood pressure response to ACE inhibition were investigated. A total of 121 patients with essential hypertension (group 1) and 125 normotensive control subjects (group 2) were included in this study. All patients were genotyped by polymerase chain reactions (PCR) for the insertion/deletion (I/D) polymorphism of the ACE gene and the M235T polymorphism of the Agt gene. To analyze possible functional impacts on blood pressure regulation 50 mg of captopril was administered to hypertensive patients. No significant association of essential hypertension with polymorphisms of the Agt and ACE gene was found. The ACE serum levels in patients with the DD-genotype of the ACE I/D polymorphism were higher than in patients with the II-genotype (P < .01). In patients with the ID-genotype the ACE serum levels were in-between. A captopril test was performed in hypertensive patients. The patients were further divided into subgroups according to the diastolic and systolic blood pressure response. Group 1a consisted of patients with a diastolic blood pressure drop of > 5 mm Hg and group 1b with < or =5 mm Hg. Group 1c consisted of patients with a systolic blood pressure drop of > 10 mm Hg and group 1d with < or =10 mm Hg. Twice as many patients with the DD genotype of the ACE gene were found in group 1a compared to group 1b (chi(2) = 5.673; P = .017). No association of systolic blood pressure change to the investigated polymorphisms was found. Our results do not support the hypothesis that the investigated polymorphisms contribute to essential hypertension. Furthermore, no major impact of these polymorphisms on blood pressure response to captopril were detected. We conclude that the investigated genotypes have no influence on blood pressure level and homeostasis.
Authors:
U F Mondorf; A Russ; A Wiesemann; M Herrero; G Oremek; T Lenz
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American journal of hypertension     Volume:  11     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  1998 Feb 
Date Detail:
Created Date:  1998-04-30     Completed Date:  1998-04-30     Revised Date:  2009-02-24    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  174-83     Citation Subset:  IM    
Affiliation:
Division of Nephrology, Medizinische Klinik IV, Johann Wolfgang Goethe Universität, Frankfurt, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
Angiotensinogen / genetics*
Captopril / therapeutic use*
Female
Genotype
Humans
Hypertension / drug therapy*,  genetics
Male
Middle Aged
Peptidyl-Dipeptidase A / blood,  genetics*
Polymorphism, Genetic*
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 11002-13-4/Angiotensinogen; 62571-86-2/Captopril; EC 3.4.15.1/Peptidyl-Dipeptidase A

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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