B2缓激肽受体（B2BKR）基因多态性与降压治疗后左心室质量变化：瑞典厄贝沙坦与阿替洛尔治疗左心室肥厚研究（SILVHIA）试验结果

B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial.

作者信息

Hallberg Pär, Lind Lars, Michaëlsson Karl, Karlsson Julia, Kurland Lisa, Kahan Thomas, Malmqvist Karin, Ohman K Peter, Nyström Fredrik, Melhus Håkan

机构信息

Department of Medical Sciences, Clinical Research Department 2, Uppsala University Hospital, 75185 Uppsala, Sweden.

出版信息

J Hypertens. 2003 Mar;21(3):621-4. doi: 10.1097/00004872-200303000-00029.

DOI:10.1097/00004872-200303000-00029

PMID:12640257

Abstract

OBJECTIVE

Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy.

DESIGN AND METHODS

We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol.

RESULTS

B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 +/- 4.6 versus -21.6 +/- 2.2 g/m2, P = 0.03).

CONCLUSIONS

Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.

摘要

目的

高血压与心血管系统的一些不良形态学和功能变化相关，包括左心室（LV）肥厚。研究表明，缓激肽通过B2缓激肽受体（B2BKR）介导可能预防LV肥厚的重要心血管效应。最近，在接受体育训练的血压正常男性中，B2BKR的+9/-9外显子1多态性与LV生长反应密切相关。我们旨在阐明在血压正常人群运动诱导的LV生长中发现的过程是否也发生在病理性LV肥厚中。