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Hypertensive left ventricular hypertrophy: relation to beta-adrenergic receptor kinase-1 (betaARK1) in peripheral
Sung-Ji Park1, Dong-Ju Choi, Choong Won Kim
1Department of Internal Medicine, College of Medicine, Gyeongsang National University, Jinju, Korea.
Background:
Left ventricular hypertrophy (LVH) is associated with increased cardiovascular risk and altered sympathetic regulation in hypertension.
Objectives:
To determine whether the level of beta-adrenergic receptor kinase-1 (betaARK1) in lymphocytes is related to LVH in patients with hypertension.
Methods:
Forty-nine patients with untreated essential hypertension were recruited to the study and classified into two groups: left ventricular hypertrophy (LVH: left ventricular mass index > or =134 g/m in men and > or =110 g/m in women; ages 52.4 +/- 12.8 years, n = 25) and non-LVH (NLVH: left ventricular mass index < 134 g/m in men and < 110 g/m in women; ages 50.8 +/- 13.1 years, n = 24). Lymphocytes were isolated from patients and quantitative-competitive reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoblotting were used to estimate the expression of betaARK1 in the lymphocytes. G-protein-coupled receptor kinase activity was assessed by rhodopsin phosphorylation assay.
Results:
The expression of betaARK1 in lymphocytes was greater in the LVH group than in the NLVH group (0.0069 +/- 0.002 ng compared with 0.0048 +/- 0.0017 ng, P < 0.01) and correlated well with left ventricular mass index (r = 0.527, P < 0.001) and relative wall thickness (r = 0.627, P < 0.001). The concentration of betaARK1 protein in lymphocytes from individuals with LVH was increased two-fold compared with that in the NLVH group (both n = 7). Lymphocyte G-protein-coupled receptor kinase activity from LVH was enhanced 1.7-fold compared with NLVH (1.03 +/- 2.16 and 1.79 +/- 1.87 pmol phosphate/min per mg protein, respectively; P < 0.05, n = 7 for each group).
Conclusions:
The concentration of betaARK1 in lymphocytes is greater in hypertensive individuals with LVH than in those without LVH and parallels the degree of hypertrophy. Generalized alterations in beta-adrenergic signalling, including betaARK1, could be a major contributory factor in the development of LVH in hypertension, and the concentration of betaARK1 in lymphocytes can reflect the development of LVH in a patient with hypertension.
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