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?1-Adrenoreceptor Polymorphisms and Blood Pressure: 49S Variant Increases Plasma Renin But Not Blood Pressure in Hypertensive Patients.


ABSTRACT: BACKGROUND:Activation of beta-1 adrenoreceptor (?1-AR) in the kidney releases renin that plays a major role in the maintenance of blood pressure. Genetic variation in ?1-AR could therefore alter the physiological and clinical effects of this hormone. We tested this hypothesis in patients from a primary care cohort being screened for primary hyperaldosteronism (n = 467). METHODS:Demographic and hemodynamic data were measured and plasma renin was determined by a standard immunoassay. Subjects were genotyped for the 2 common single-nucleotide polymorphisms Arg389Gly (rs1801253) and Ser49Gly (rs1801252), and thus the 4 possible haplotypes in ?1-AR gene. RESULTS:In patients being screened for hyperaldosteronism, plasma renin was significantly elevated in Ser49 homozygotes (49SS) compared with Gly49 (49G) allele carriers (0.307 ± 0.03 vs. 0.164 ± 0.05; P = 0.01). However, this did not translate into differences in either blood pressure or heart rate. On the other hand, the Arg389Gly polymorphism did not affect either plasma renin or blood pressure in this group. There was also no evidence that the 2 loci were linked in this group of patients. CONCLUSION:These data suggest that in this cohort the Ser49 variant of the Ser49Gly ?1-AR gene polymorphism associates with higher renin levels. However, these common ?1-AR gene polymorphisms do not affect blood pressure in the same cohort.

SUBMITTER: Sandilands AJ 

PROVIDER: S-EPMC6475877 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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β1-Adrenoreceptor Polymorphisms and Blood Pressure: 49S Variant Increases Plasma Renin But Not Blood Pressure in Hypertensive Patients.

Sandilands Alastair J AJ   O'Shaughnessy Kevin M KM  

American journal of hypertension 20190401 5


<h4>Background</h4>Activation of beta-1 adrenoreceptor (β1-AR) in the kidney releases renin that plays a major role in the maintenance of blood pressure. Genetic variation in β1-AR could therefore alter the physiological and clinical effects of this hormone. We tested this hypothesis in patients from a primary care cohort being screened for primary hyperaldosteronism (n = 467).<h4>Methods</h4>Demographic and hemodynamic data were measured and plasma renin was determined by a standard immunoassay  ...[more]

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