Beta-2 adrenergic receptor polymorphisms and blood pressure responses to salt

Abstract

The genetic basis for salt-sensitive hypertension is not known. Altered regulatory mechanisms such as vascular reactivity and/or sodium excretion are thought to contribute to salt sensitivity. Linkage analysis indicates that the blood pressure response to sodium loading is associated with the beta-2 adrenergic receptor (BAR2) locus suggesting that this gene may be an important regulator of blood pressure responses to salt. The common Arg16Gly and Gln27Glu BAR2 polymorphisms have been associated with enhanced agonist mediated desensitization and increased agonist-mediated responsiveness, respectively but their effects on salt sensitivity are not known. Healthy subjects (n = 23) received a high (400meq) and a low (10meq) salt diet for 5 days in random order. Automated blood pressure monitoring was performed on the last day of each diet. The change in blood pressure between low and high salt days was calculated and compared among genotypes. There was no significant genotypic difference in salt induced changes in systolic (Arg16Gln27[n = 8] 2.3 ± 3.8 mmHg, Gly16Gln27 [n = 7] 3.1 ± 3.3 mmHg and Gly16Glu27 [n = 8] 6.1 ± 2.8 mmHg: P = 0.66) or diastolic (Arg16Gln27 −2.4 ± 1.7 mmHg, Gly16Gln27 1.1 ± 1.6 mmHg and Gly16Glu27 −1.5 ± 1.2 mmHg: P = 0.26) blood pressure. These findings suggest that the BAR2 Arg16Gly and Gln27Glu polymorphisms are not a significant determinant of blood pressure responses to salt. Clinical Pharmacology & Therapeutics (2004) 75, P13–P13; doi: 10.1016/j.clpt.2003.11.048