Renin-angiotensin-aldosterone system and G-protein beta-3 subunit gene polymorphisms in salt-sensitive essential hypertension

• Published in: Journal of human hypertension Vol. 17; no. 3; pp. 187 - 191
• Main Authors: Pamies-Andreu, E, Ramirez-Lorca, R, Stiefel García-Junco, P, Muñiz-Grijalbo, O, Vallejo-Maroto, I, Garcia Morillo, S, Miranda-Guisado, M L, Ortíz, J V, Carneado de la Fuente, J
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.03.2003; Nature Publishing Group
• Subjects: Adult; Aldosterone; Aldosterone - blood; Aldosterone synthase; Alleles; Angiotensin; Angiotensin II; Blood pressure; Blood Volume - physiology; Epidemiology; Female; G proteins; Gene polymorphism; Genetic aspects; Genotype; Health Administration; Heterotrimeric GTP-Binding Proteins - genetics; Heterotrimeric GTP-Binding Proteins - physiology; Humans; Hypertension; Hypertension - chemically induced; Hypertension - genetics; Hypertension - physiopathology; Insertion; Male; Medicine; Medicine & Public Health; original-article; Peptidyl-dipeptidase A; Physiological aspects; Polymerase chain reaction; Polymorphism; Polymorphism, Genetic - physiology; Protein G; Proteins; Public Health; Renin; Renin - blood; Renin-angiotensin system; Renin-Angiotensin System - genetics; Renin-Angiotensin System - physiology; Salt; Sodium Chloride, Dietary - adverse effects; Sodium Chloride, Dietary - metabolism; Spain; aldosterone synthase; genetic polymorphisms; renin–angiotensin system; salt sensitivity; protein G
• ISSN: 0950-9240; 1476-5527
• DOI: 10.1038/sj.jhh.1001534

Approximately 50% of hypertensive patients are salt sensitive (they increase their Blood Pressure in response to sodium intake or volume expansion). Mechanisms underlying salt sensitivity are not completely elucidated although there is evidence that they may be genetically determined. The aim of this study is to establish the relation among some genetic polymorphisms of the renin–angiotensin system (RAAS) and the beta-3 subunit of the protein G and salt sensitivity. We studied 102 essential hypertensive patients, stage 1–2 and without target organ damage. Salt sensitivity was assessed by the rapid protocol of Weinberger. We determined by polymerase Chain reaction techniques the following polymorphisms: insertion/deletion (I/D) of the angiotensin-converting enzyme (ACE), A1166C of the angiotensin II type 1 receptor (AT1R), −344C/T and intron 2 conversion (IC) of the aldosterone synthase (CYP11B2), and C825T of the beta-3 subunit of the protein G (GNB3). 41 patients (40.19%) were salt sensitive. The distribution of the different polymorphisms was similar in both groups of patients, but subjects carriers of the W allele of the CYP11B2 IC polymorphism had a greater risk for salt sensitivity as compared with no carriers (37 of 41, 90.2% vs 4 of 41, 9.8%, OR 3.02, P <0.05). Although there is no association between salt sensitivity and the different studied genotypes of the RAAS and of the GNB3, our data show a greater risk for salt sensitivity among carriers of the W allele of the CYP11B2 1C polymorphism.