Early Inflammatory and Metabolic Changes in Association With AGTR1 Polymorphisms in Prehypertensive Subjects
| العنوان: | Early Inflammatory and Metabolic Changes in Association With AGTR1 Polymorphisms in Prehypertensive Subjects |
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| المؤلفون: | Sushi I. K. Mahata, Daniel T. O'Connor, Sameer Poddar, Manjula Mahata, Srikrishna Khandrika, Maple M. Fung, Fangwen Rao |
| المصدر: | American Journal of Hypertension. 24:225-233 |
| بيانات النشر: | Oxford University Press (OUP), 2011. |
| سنة النشر: | 2011 |
| مصطلحات موضوعية: | Adult, Blood Glucose, Leptin, Male, Candidate gene, medicine.medical_specialty, Blood Pressure, Fatty Acids, Nonesterified, Risk Assessment, California, Receptor, Angiotensin, Type 1, Article, Prehypertension, Young Adult, Gene Frequency, Risk Factors, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Humans, Insulin, Genetic Predisposition to Disease, Least-Squares Analysis, Inflammation, Polymorphism, Genetic, biology, Interleukin-6, business.industry, C-reactive protein, Middle Aged, medicine.disease, Angiotensin II, C-Reactive Protein, Cholesterol, Phenotype, Endocrinology, Blood pressure, Pathophysiology of hypertension, biology.protein, Female, Inflammation Mediators, Metabolic syndrome, business, Biomarkers |
| الوصف: | Cardiovascular and all-cause mortality is directly related to blood pressure, even for blood pressure as low as 115/75 mm Hg.1 Given increased disease risk even in subjects with “high-normal” blood pressures, the Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) 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.2 Many of the pathophysiologic mechanisms that play a role in hypertension may already be deranged in prehypertensive subjects,3 including inflammatory pathways that result in elevated C-reactive protein (CRP)4 and interleukin-6 (IL-6),5 as well as metabolic pathways that result in elevated glucose and insulin levels.6 However, conclusions are often confounded due to obesity and presence of the metabolic syndrome and other cardiovascular disease risk factors. Undoubtedly, hypertension is influenced by heredity with family history highly predictive of future hypertension. Large genome-wide association studies have revealed principally minor associations7 perhaps not surprising in light of a number of challenges including the definition of hypertension used.8 Despite the continuum of disease and cardiovascular risk with blood pressure, few studies have investigated genetic influences in prehypertensive subjects. Candidate genes from the renin–angiotensin system (RAS) pathway, which play a primary role in vascular tone, hypertension, and sodium and water excretion, have been implicated as contributors to genetic hypertension. In particular, the angiotensin II receptor type-1 gene (AGTR1)9 has been frequently studied given that its gene product is the primary receptor for angiotensin II, especially in the heart and the kidney. AGTR1, a G-protein coupled receptor, is the target of pharmacologic intervention and has been studied in a number of medical conditions including heart failure10 and stroke.11 The A1166C polymorphism in the 3′-untranslated region (UTR) of the gene, which affects receptor expression,12 has been extensively investigated in hypertension,13 but there is also evidence that it influences the metabolic syndrome.14 Hypertension has previously been associated with inflammation and metabolic changes as well as common AGTR1 genetic polymorphisms. The aim of our study was to determine whether such changes and genetic polymorphisms are noted in young prehypertensive subjects, who do not yet have evidence of diabetes or cardiovascular disease. |
| تدمد: | 1941-7225 0895-7061 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::14a6f32653d3bc5dd49a458d4c8041c7Test https://doi.org/10.1038/ajh.2010.210Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....14a6f32653d3bc5dd49a458d4c8041c7 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19417225 08957061 |
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