Document Detail

Blood pressure in patients with primary aldosteronism is influenced by bradykinin B(2) receptor and alpha-adducin gene polymorphisms.
MedLine Citation:
PMID:  12107246     Owner:  NLM     Status:  MEDLINE    
Primary aldosteronism (PA) is the most common cause of endocrine hypertension. PA is most frequently presented as moderate to severe hypertension, but the clinical and biochemical features vary widely. The aim of our study was to identify genetic variants that influence the phenotype of patients with PA. We hypothesized that genetic variants potentially affecting aldosterone production (aldosterone synthase, CYP11B2), renal proximal tubule reabsorption (alpha-adducin), or the mechanisms of counterbalance leading to vasodilatation and sodium excretion (bradykinin B(2)-receptor, B(2)R) could influence the clinical and biochemical characteristics of patients with PA. We studied three polymorphisms of these genes (C-344T of CYP11B2, G460W of alpha-adducin, and C-58T of B(2)R) in 167 primary aldosteronism patients (56 with aldosterone-producing adenoma and 111 with idiopathic hyperaldosteronism). B(2)R and alpha-adducin genotypes were strong independent predictors of both systolic and diastolic blood pressure levels; plasma renin activity and aldosterone also play a marginal role on BP levels. Body mass index, age, sex, and CYP11B2 genotype displayed no significant effect on the clinical parameters of our population. In particular, alpha-adducin and B(2)R polymorphisms accounted for 13.2% and 11.0% of the systolic and diastolic blood pressure variance, respectively. These data suggest that genetic variants of alpha-adducin and the bradykinin B(2)-R influence the blood pressure levels in patients with primary aldosteronism.
Paolo Mulatero; Tracy A Williams; Alberto Milan; Cristina Paglieri; Franco Rabbia; Francesco Fallo; Franco Veglio
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  87     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-07-10     Completed Date:  2002-08-02     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3337-43     Citation Subset:  AIM; IM    
Department of Medicine and Experimental Oncology, Hypertension Unit, San Vito Hospital, University of Turin, Strada San Vito 34, 10133 Turin, Italy.
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MeSH Terms
Aldosterone Synthase / genetics
Blood Pressure*
Calmodulin-Binding Proteins / genetics*
Hyperaldosteronism / genetics*,  physiopathology*
Infant, Newborn
Polymorphism, Genetic* / physiology
Receptor, Bradykinin B2
Receptors, Bradykinin / genetics*
Regression Analysis
Reg. No./Substance:
0/Calmodulin-Binding Proteins; 0/Receptor, Bradykinin B2; 0/Receptors, Bradykinin; 0/adducin; EC Synthase

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