| Early inflammatory and metabolic changes in association with AGTR1 polymorphisms in prehypertensive subjects. | |
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MedLine Citation:
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PMID: 20864943 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure in 2003 created a prehypertension category for persons with blood pressures ranging from systolic blood pressure (SBP) of 120-139 mm Hg or diastolic blood pressure (DBP) from 80 to 89 mm Hg, due to increased risk of cardiovascular disease. METHODS: Our study utilized the University of California-San Diego (UCSD) Twin Hypertension Cohort. We measured comprehensive plasma cholesterol levels and metabolic (glucose, insulin, leptin) and inflammatory markers (interleukin-6 (IL-6), C-reactive protein (CRP), free fatty acids) to determine the differences between normotensive and prehypertensive subjects. Additionally, we determined whether angiotensin II receptor type-1 (AGTR1) polymorphisms, previously associated with hypertension, could predict prehypertension. RESULTS: A total of 455 white subjects were included in the study (mean age 37.1 years). Prehypertensive subjects were older with greater body mass index (BMI) than the normotensives, and after adjusting for sex and age, had greater plasma glucose, insulin, and IL-6. The common AGTR1 A1166C (rs5186) polymorphism in the 3'-UTR region, particularly the presence of the 1166C allele, which fails to downregulate gene expression, predicted greater likelihood of being in the prehypertension group and higher SBP. A lesser-studied polymorphism in intron-2 of AGTR1 (A/G; rs2276736) was associated with plasma high-density lipoprotein (HDL) and apolipoprotein A-1. In a subgroup analysis of nonobese subjects (N = 405), similar associations were noted. CONCLUSION: Prehypertensive subjects already exhibit early pathophysiologic changes putting them at risk of future cardiovascular disease, and AGTR1 may also contribute to this increased risk. Further investigation is needed to confirm these findings and the precise molecular mechanisms of action. |
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Authors:
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Maple M Fung; Fangwen Rao; Sameer Poddar; Manjula Mahata; Srikrishna Khandrika; Sushil K Mahata; Daniel T O'Connor |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Twin Study Date: 2010-09-23 |
Journal Detail:
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Title: American journal of hypertension Volume: 24 ISSN: 1941-7225 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-01-20 Completed Date: 2011-05-03 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 225-33 Citation Subset: IM |
Affiliation:
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Veterans Affairs San Diego Healthcare System, La Jolla, California, USA. mafung@ucsd.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Biological Markers / blood Blood Glucose / analysis Blood Pressure / genetics* C-Reactive Protein / analysis California Cholesterol / blood Fatty Acids, Nonesterified / blood Female Gene Frequency Genetic Predisposition to Disease Humans Inflammation / blood, genetics*, immunology Inflammation Mediators / blood Insulin / blood Interleukin-6 / blood Least-Squares Analysis Leptin / blood Male Middle Aged Phenotype Polymorphism, Genetic* Prehypertension / blood, genetics*, immunology, physiopathology Receptor, Angiotensin, Type 1 / genetics* Risk Assessment Risk Factors Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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MD00020/MD/NCMHD NIH HHS; P01 HL058120-10/HL/NHLBI NIH HHS; P60 MD000220-10/MD/NCMHD NIH HHS; RR00827/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/AGTR1 protein, human; 0/Biological Markers; 0/Blood Glucose; 0/Fatty Acids, Nonesterified; 0/IL6 protein, human; 0/Inflammation Mediators; 0/Interleukin-6; 0/Leptin; 0/Receptor, Angiotensin, Type 1; 11061-68-0/Insulin; 57-88-5/Cholesterol; 9007-41-4/C-Reactive Protein |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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