CAJ | 학술논문

目的研究Gαq/11介导的信号转导通路在2K1C肾性高血压大鼠心脏和主动脉中的变化以及卡托普利治疗对其的影响. 方法制备2K1C肾性高血压大鼠模型, 于术后4～8周给予卡托普利(150 mg/kg),观察尾动脉收缩压、左室重与体重之比和主动脉形态学改变.测定心脏和主动脉中Gαq/11含量和磷脂酶C(PLC)活性. 结果 2K1C肾性高血压大鼠在术后4周和8周出现明显的高血压、心肌肥大和主动脉增厚, 心脏和主动脉中Gαq/11含量明显增加.卡托普利治疗4周可以降低血压并逆转心肌肥大, 心脏Gαq/11含量及PLC活性分别降低了15.8%和30.9%, 而主动脉中Gαq/11含量及PLC活性均无变化. 结论 Gαq/11介导的信号转导通路参与2K1C肾性高血压的发生和维持.卡托普利可以逆转心肌肥大, 这一作用可能是通过抑制血管紧张素Ⅱ(Ang Ⅱ)的生成从而消除 Ang Ⅱ导致的Gαq/11介导的信号转导通路的激活而实现的.
목적연구Gαq/11개도적신호전도통로재2K1C신성고혈압대서심장화주동맥중적변화이급잡탁보리치료대기적영향. 방법제비2K1C신성고혈압대서모형, 우술후4～8주급여잡탁보리(150 mg/kg),관찰미동맥수축압、좌실중여체중지비화주동맥형태학개변.측정심장화주동맥중Gαq/11함량화린지매C(PLC)활성. 결과 2K1C신성고혈압대서재술후4주화8주출현명현적고혈압、심기비대화주동맥증후, 심장화주동맥중Gαq/11함량명현증가.잡탁보리치료4주가이강저혈압병역전심기비대, 심장Gαq/11함량급PLC활성분별강저료15.8%화30.9%, 이주동맥중Gαq/11함량급PLC활성균무변화. 결론 Gαq/11개도적신호전도통로삼여2K1C신성고혈압적발생화유지.잡탁보리가이역전심기비대, 저일작용가능시통과억제혈관긴장소Ⅱ(Ang Ⅱ)적생성종이소제 Ang Ⅱ도치적Gαq/11개도적신호전도통로적격활이실현적.
Objective To investigate the alteration of Gαq/11-mediated signal transduction pathway in heart and aorta of 2K1C renal hypertensive rats and the effect of captopril treatment. Methods Renal hypertension was performed by placing a sliver clip around the left renal artery. Captopril (150 mg/kg) was given from 4 to 8 weeks after operation. Systolic blood pressure was recorded by the tail-cuff method each week after surgery, the ratio of left ventricular weight to body weight (LV/BW) and morphologic changes in aorta were measured at 4 and 8 weeks after operation. The levels of Gαq/11 in heart and aorta were detected by Western Blot analysis, and phospholipase C (PLC) activities were determined by using [3H] PIP2 as substrate. Results 2K1C renal hypertensive rats had significant hypertension, cardiac hypertrophy and aorta thickening 4 and 8 weeks after operation. Systolic blood pressure and the LV/BW decreased to the level of sham group 4 weeks after captopril treatment while the morphologic change in aorta was not significant. For 2K1C group, Gαq/11 levels and PLC activities increased dramatically both in heart and in aorta at 4 weeks that remained at high levels until 8 weeks after the operation. After captopril treatment, the Gαq/11 level and PLC activity in heart decreased by 15.8% and 30.9% respectively with no changes in aorta. Conclusion Gαq/11-mediated signal transduction pathway participated in the development and maintain of 2K1C renal hypertension. Captopril reversed cardiac hypertrophy and this effect may be attributed by inhibiting the formation of angiotensin Ⅱ and, therefore, abolishing the activation of Gαq/11-mediated signal transduction pathway induced by angiotensin Ⅱ.