Objective: The objective of our work was to analyze if changes in the expression of beta-adrenoceptors (beta-ARs) and G-protein-coupled receptor kinases (GRKs) in human lymphocytes - a practical surrogate for myocardial or vascular cells - are related to the hypertensive state and its clinical consequences.
Methods: Real-time quantitative RT-PCR was employed to evaluate the expression of the three beta-ARs (beta1, beta2, beta3) and three GRKs (GRK2, GRK3, GRK5) in human lymphocytes obtained from both normotensive and hypertensive patients, some of whom had been treated with blockers of the renin-angiotensin system. Office blood pressure, 24-h ambulatory blood pressure, urinary albumin excretion and serum biochemical profile were also recorded.
Results and conclusions: beta1-AR expression levels were higher in circulating lymphocytes from hypertensive patients (2-DeltaDeltaCt = 2.135 +/- 0.4252*, vs. control group), but this difference was not observed when these patients were treated with blockers of the renin-angiotensin system. beta1-AR levels directly correlated (r2 = 0.5711, P = 0.0185) with urinary albumin excretion in microalbuminuric patients, which relates alterations of this receptor to cardiovascular risk. An inverse correlation was observed between the expression levels of beta2-AR and diastolic blood pressure (r2 = 0.2078, P = 0.0031), suggesting that beta2-AR levels in lymphocytes mirror their expression in vascular cells, in which beta2-AR-mediated relaxation regulates vascular resistance. mRNA levels for GRK3 were inversely correlated with systolic and diastolic blood pressure (day, night and 24 h), which suggests a protective role for GRK3 in the regulation of human blood pressure, as supported by previous findings in transgenic mice.