Clinica Medica 4, Department of Clinical and Experimental Medicine, University of Padua, Padua, Italy.
J Hypertens. 2010 May;28(5):1104-8. doi: 10.1097/HJH.0b013e328339930f.
RGS2 (regulators of G-protein signalling) is a negative regulator of Galphaq protein signalling, which mediates the action of several vasoconstrictors. Low RGS2 expression increases G-protein-coupled signalling in hypertensive patients. The aim of the present study was to correlate RGS2 expression in peripheral blood mononuclear cells (PBMs) with response to antihypertensive therapy in never-treated patients with essential hypertension.
RGS2 expression was measured by real-time quantitative RT-PCR in peripheral blood mononuclear cells (PBMs) from 102 essential hypertensives. The diagnosis of essential hypertension was based on all clinically required tests, including the captopril suppression test. Antihypertensive treatment was given in accordance to international guidelines. End-point of the study was systolic blood pressure (BP) less than 140 mmHg and diastolic BP less than 90 mmHg with three or less different antihypertensive agents, which identified responders to treatment. Resistant hypertension was defined as the failure to control systolic and/or diastolic BP despite at least three different classes of antihypertensive agents, including a diuretic.
During follow-up, 85 (83%) patients reached the end point (responders). Resistant hypertensives (n = 17, 17%) were older, had higher baseline BP, plasma aldosterone and aldosterone: renin ratio (ARR) and lower plasma renin activity than patients who reached the end point. RGS2 was negatively correlated to systolic BP at enrollment and significantly lower in PBMs from resistant hypertensives in comparison with patients that reached BP goal. According to logistic regression analysis, high RGS2 expression was predictor of reaching BP goal, whereas high ARR after captopril, age and systolic pressure at enrolment were predictor of resistant hypertension.
RGS2 expression affects the response to antihypertensive treatment. Reduced RGS2 expression contributes to resistance to antihypertensive agents through poor negative feedback on the effects of aldosterone and of other vasoactive agents.
RGS2（G 蛋白信号转导调节因子）是 Galphaq 蛋白信号转导的负调节剂，介导几种血管收缩剂的作用。低 RGS2 表达增加高血压患者的 G 蛋白偶联信号转导。本研究的目的是将外周血单个核细胞（PBMs）中的 RGS2 表达与未经治疗的原发性高血压患者对降压治疗的反应相关联。
通过实时定量 RT-PCR 测量 102 例原发性高血压患者外周血单个核细胞（PBMs）中的 RGS2 表达。原发性高血压的诊断基于所有临床必需的检查，包括卡托普利抑制试验。根据国际指南给予降压治疗。研究的终点是收缩压（BP）<140mmHg 和舒张压（BP）<90mmHg，使用三种或更少的不同降压药物，这可以确定治疗的反应者。难治性高血压定义为尽管使用了至少三种不同类别的降压药物，包括利尿剂，但仍无法控制收缩压和/或舒张压。
在随访期间，85 例（83%）患者达到终点（反应者）。难治性高血压患者（n=17，17%）年龄较大，基线 BP、血浆醛固酮和醛固酮：肾素比值（ARR）较高，血浆肾素活性较低，与达到 BP 目标的患者相比。RGS2 与入组时的收缩压呈负相关，并且在难治性高血压患者的 PBMs 中明显低于达到 BP 目标的患者。根据逻辑回归分析，高 RGS2 表达是达到 BP 目标的预测因子，而卡托普利后 ARR、年龄和入组时的收缩压是难治性高血压的预测因子。
RGS2 表达影响降压治疗的反应。RGS2 表达减少通过对醛固酮和其他血管活性物质的作用的负反馈不良，导致对降压药物的耐药性。
