Document Detail


Beta-2 adrenergic receptor diplotype defines a subset of salt-sensitive hypertension.
MedLine Citation:
PMID:  17015767     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Two genetic variants of the beta-2 adrenergic receptor, 46G>A and 79C>G, affect agonist-mediated receptor downregulation and vascular reactivity. We determined whether these variants were associated with hypertension, per se, blood pressure response to dietary sodium, 2 forms of salt-sensitive hypertension (low renin and nonmodulation), and the activity of the renin-angiotensin-aldosterone system. Included are 280 hypertensive and 65 normotensive white subjects who had the 2 beta-2 adrenergic receptor genotypes available. Of all subjects, 171 hypertensive and 48 normotensive subjects had complete data for intermediate phenotyping and blood pressure evaluation on high- and low-sodium balance. The beta-2 adrenergic receptor variants were not associated with hypertension per se. However, among hypertensive subjects, the change (from low to high sodium balance) in mean arterial pressure differed significantly by genotype and by diplotype. Compared with all of the other diplotypes combined, 46AA/79CC was associated with a greater change in blood pressure. Furthermore, this diplotype was associated with low-renin (LR) hypertension (identifying 32% of the LR hypertensives), higher plasma aldosterone, and lower plasma renin and serum potassium levels. In conclusion, the 46AA/79CC diplotype is associated with greater blood pressure response to dietary sodium and higher odds of LR hypertension. We propose that the mechanism for the observed association is inadequate suppression of aldosterone with salt intake, implicating the beta-2 adrenergic receptor in the regulation of aldosterone secretion. This hypothesis was confirmed in isolated glomerulosa cells, where beta-2 adrenergic receptor stimulation increased aldosterone secretion, whereas blockade reduced the stimulated aldosterone response. Importantly, this association could only be detected with an intermediate and not a distant phenotype.
Authors:
Luminita Pojoga; Nikheel S Kolatkar; Jonathan S Williams; Todd S Perlstein; Xavier Jeunemaitre; Nancy J Brown; Paul N Hopkins; Benjamin A Raby; Gordon H Williams
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-10-02
Journal Detail:
Title:  Hypertension     Volume:  48     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-20     Completed Date:  2006-12-11     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  892-900     Citation Subset:  IM    
Affiliation:
Brigham and Women's Hospital, Division of Endocrinology, Diabetes, and Hypertension, 221 Longwood Ave, Boston, MA 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Animals
Female
Genetic Variation
Humans
Hypertension / chemically induced,  genetics*,  metabolism
Middle Aged
Phenotype
Polymorphism, Genetic
Rats
Rats, Wistar
Receptors, Adrenergic, beta-2 / genetics*,  physiology
Sodium Chloride, Dietary*
Grant Support
ID/Acronym/Agency:
DK63214/DK/NIDDK NIH HHS; HL069208/HL/NHLBI NIH HHS; HL47651/HL/NHLBI NIH HHS; HL59424/HL/NHLBI NIH HHS; M01RR00064/RR/NCRR NIH HHS; M01RR00095/RR/NCRR NIH HHS; M01RR02635/RR/NCRR NIH HHS; P50HL055000/HL/NHLBI NIH HHS; T32HL007609/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic, beta-2; 0/Sodium Chloride, Dietary
Comments/Corrections
Comment In:
Hypertension. 2006 Nov;48(5):820-1   [PMID:  17015779 ]

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


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