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目的探讨血管紧张素(1-7)[Ang(1-7)]对单纯压力负荷增加及肾素-血管紧张素-醛固酮系统(RAAS)激活的高血压模型左右心室收缩及舒张功能的影响及其机制。方法建立肾下主动脉缩窄(INAC)及二肾一夹(2K1C)模型,应用微渗泵植入技术,使Ang(1-7)进行不同时间(14及28d)的体内干预,采用经颈动脉插入心导管法检测这两种高血压模型左室和右室收缩及舒张功能。结果在2K1C动物模型,建模同时及术后14d应用Ang(1-7),均可有效降低血压,平均下降15%～20%(P<0.05)。在INAC动物模型,建模同时应用Ang(1-7),在术后第14天时血压下降13.6%(P<0.05);术后14d开始应用Ang(1-7),血压下降7.9%。在2K1C模型,14d时其左室收缩功能无明显变化,但其舒张功能则已受损,Ang(1-7)可使其显著改善(-dp/dtmax,P<0.05);术后42d,2K1C组的收缩与舒张功能均明显受损;Ang(1-7)可使其收缩功能显著改善(+dp/dtmax,P<0.05),但对其舒张功能则改善不明显(-dp/dtmax,LVDEP)。在2K1C模型的右室,14d时收缩及舒张功能均已受损,Ang(1-7)可使其显著改善[2K1C组比Ang(1-7)组,+dp/dtmax,-dp/dtmax,P<0.05];术后第42天,右室的收缩与舒张功能受损更为明显,Ang(1-7)使其收缩功能显著改善(+dp/dtmax,P<0.05),对其舒张功能则改善不明显(-dp/dtmax)。在INAC动物模型,14d时其左室收缩和舒张功能均无明显变化;42d时,其舒张功能有所降低(-dp/dtmax,P<0.05),Ang(1-7)可使其明显改善(-dp/dtmax,P<0.05)。14及42d时,其右室收缩与舒张功能均无明显变化,Ang(1-7)对其亦无明显影响。结论Ang(1-7)可改善高血压模型左室和右室收缩及舒张功能。但对两种模型的改善程度不同,且与其降压效果不同步,提示Ang(1-7)对心功能的改善可能具有多种作用机制。
Objective To investigate the effects of angiotensin (1-7) [Ang (1-7)] on left and right ventricular systolic and diastolic function in hypertensive rats induced by simple pressure overload and hypertension induced by renin-angiotensin-aldosterone system (RAAS) Its mechanism. Methods The models of INAC and 2K1C were established. The micro-osmotic pump implantation technique was used to make Ang (1-7) in vivo intervention at different time (14 and 28 days) Carotid artery catheterization was used to detect left ventricular and right ventricular systolic and diastolic function in both hypertension models. Results Both 2K1C animal models and the application of Ang (1-7) at the same time and 14 days after operation were effective in lowering blood pressure with an average decrease of 15% -20% (P <0.05). In INAC animal model, Ang (1-7) was applied at the same time. The blood pressure decreased 13.6% (P <0.05) on the 14th day after operation. In the 2K1C model, there was no significant change in left ventricular systolic function at 14 days, but diastolic function was impaired, Ang (1-7) significantly improved (-dp / dtmax, P <0.05) The contraction and diastolic function of 2K1C group were significantly impaired; Ang (1-7) significantly improved the systolic function (+ dp / dtmax, P <0.05), but did not improve the diastolic function (-dp / dtmax , LVDEP). In the 2K1C model right ventricle, systolic and diastolic functions were impaired at 14 days and Ang (1-7) significantly improved [2K1C group compared with Ang (1-7) group, + dp / dtmax, -dp / dtmax , P <0.05]. Right ventricular systolic and diastolic dysfunction was more obvious on the 42nd day after operation, Ang (1-7) significantly improved the systolic function (+ dp / dtmax, P <0.05) Diastolic function was not significantly improved (-dp / dtmax). In the animal model of INAC, the left ventricular systolic and diastolic function did not change significantly on the 14th day, and the diastolic function was decreased on the 42th day (-dp / dtmax, P <0.05). Ang (1-7) (-dp / dtmax, P <0.05). At 14 and 42 days, there was no significant change in systolic and diastolic function of right ventricle, Ang (1-7) had no significant effect on it. Conclusion Ang (1-7) can improve left ventricular systolic and diastolic function in hypertensive rats. However, the improvement of the two models is different, and its antihypertensive effect is not synchronized, suggesting that Ang (1-7) may have a variety of mechanisms for improving cardiac function.