高盐负荷对大鼠血管紧张素Ⅱ（AⅡ）受体mRNA表达的影响

EFFECTS OF HIGH SALT-LOADING ON THE REGULATION OF ANGIOTENSIN Ⅱ RECEPTOR mRNA EXPRESSION

本实验采用逆转录──聚合酶链式反应（ＲＴ－ＰＣＲ）技术，比较了１２周龄卒中型自发性高血压大鼠（ＳＨＲｓｐ）和正常血压大鼠（ＷＫＹ）主动脉平滑肌、心室肌和肾上腺等组织的血管紧张素Ⅱ受体的１ａ亚型（ＡＴ１ａ）和１ｂ亚型（ＡＴ１ｂ）ｍＲＮＡ的表达，同时检测了高盐负荷对两种大鼠ＡＴ１ａ和ＡＴ１ｂ受体ｍＲＮＡ表达的影响。结果显示：（１）在ＳＨＲｓｐ，ＡＴ１ａ和ＡＴ１ｂｍＲＮＡ在肾上腺的表达明显高于ＷＫＹ大鼠（分别高１７６％和１５７％），其它组织的表达均低于ＷＫＹ大鼠（在主动脉平滑肌分别低１０％和２３％，在心室肌分别低２３％和４０％）。（２）高盐负荷后，ＷＫＹ大鼠肾上腺的ＡＴ１ａ和ＡＴ１ｂ及心室肌的ＡＴ１ｂｍＲＮＡ的表达显著增加（在肾上腺分别高１６７％和４０１％，在心室肌高６２％），主动脉平滑肌ＡＴ１ａ和ＡＴ１ｂ及心室肌ＡＴ１ａｍＲＮＡ的表达未见明显改变。（３）高盐负荷后，ＳＨＲｓｐ主动脉平滑肌的ＡＴ１ｂ及心室肌的ＡＴ１ａ和ＡＴ１ｂｍＲＮＡ的表达均显著增高（在主动脉平滑肌高９０％，在心室肌分别高５９０％和２００％），肾上腺的ＡＴ１ａｍＲＮＡ的表达明显下降（下降５８％），主动脉平滑肌的ＡＴ１ａ及肾上腺的ＡＴ１ｂｍＲＮＡ的?

In the present study, the angiotensin Ⅱ receptor subtype Ⅰ-a (AT1a) and Ⅰ-b (AT1b ) mRNA levels in aortic smooth muscle (ASM ), ventricular myocardium (VM) and adrenal from 1 2- week- old stroke-prone spontaneously hypertensive rats (SHRsp) and age-matched Wistar-Kyoto (WKY) rats with normal diet (control) and high salt-loading were examined by reverse transcriptase-polymerase chain reaction (RT-PCR). The results showed that: (1 ) The AT1 a and AT1b mRNA levels in ASM and VM from SHRsp were lower than those from WKY rats (in ASM, 10% and 23 %, while in VM, 23 % and 4 0 % lower, respectively). In contrast, both AT1a and AT1b mRNA levels in adrenal from SHRsp were higher (1 76 % and 1 57 %, respectively ). (2) In the WKY rats with high salt-loading, the AT1a and AT1b mRNA levels in adrenal, as well as AT1 b mRNA level in VM, increased significantly, as compared with the control (in adrenal, 1 67% and 401 %, while in VM, 62 % ). However, the AT1a and AT1b mRNA levels in ASM, as well as AT1a mRNA level in VM, showed no obvious change. (3 ) In SHRsp with high salt-loading, the AT1b mRNA level in ASM, as well as AT1a and AT1b mRNA levels in VM, increased markedly (in ASM,90 %, while in VM, 590 % and 200 % ); whereas the AT1a mRNA level in adrenal decreased significantly (58% ). There was little influence on the regulation of AT1a (in ASM) and AT1b (in adrenal) receptor gene expression after high salt-loading. The resuits suggest that AT 1 a and AT1b receptors may be involved in the pathogenesis of saltinduced hypertension. The up-regulation of AT1b receptors in ASM may induce the remodeling of arterial wall, while that of AT1a and AT1b receptors in VM might contribute to ventricular hypertrophy in hypertension. Furthermore, there are certain differences between SHRsp and WKY rats with respect to the regulation of AT1a and AT1b receptor gene expression with or without external stimulation.