| 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 |
Abstract/OtherAbstract:
|
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. |
| | |
Authors:
|
Paolo Mulatero; Tracy A Williams; Alberto Milan; Cristina Paglieri; Franco Rabbia; Francesco Fallo; Franco Veglio |
Related Documents
:
|
18347776 - Spironolactone for poorly controlled hypertension in type 2 diabetes: conflicting effec... 3896046 - Essential hypertension: a metabolic cause? a hypothesis. 10474126 - Aldosterone-producing adenoma without hypertension: a report of two cases. 15133306 - Combined adrenal myelolipoma and medullary hyperplasia. 18551006 - Validation of brachial artery pressure reconstruction from finger arterial pressure. 21685736 - Beds: practical pressure management for surfaces/mattresses. |
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 |
Affiliation:
|
Department of Medicine and Experimental Oncology, Hypertension Unit, San Vito Hospital, University of Turin, Strada San Vito 34, 10133 Turin, Italy. paolo.mulatero@libero.it |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Aldosterone Synthase
/
genetics Blood Pressure* Calmodulin-Binding Proteins / genetics* Female Genotype Humans Hyperaldosteronism / genetics*, physiopathology* Infant, Newborn Male Polymorphism, Genetic* / physiology Receptor, Bradykinin B2 Receptors, Bradykinin / genetics* Regression Analysis |
| Chemical | |
Reg. No./Substance:
|
0/Calmodulin-Binding Proteins; 0/Receptor, Bradykinin B2; 0/Receptors, Bradykinin; 0/adducin; EC 1.14.15.4/Aldosterone Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-h...
Next Document: Novel mutations responsible for autosomal recessive multisystem pseudohypoaldosteronism and sequence...