ADM对LNNA诱导的高血压心肌肥大的作用及机制探讨

本工作在ＬＮＮＡ经慢性ＮＯ封闭诱导的大鼠高血压心肌肥大模型上研究了ＡＤＭ对其心肌肥大和Ｍ５ＬＶ钠一钙交换功能损伤的作用。结果：一、较之对照组，ＬＮＮＡ组ＭＡＯ和ＬＶＩ分别增加５７．４％和１８。０％（Ｐ＜０．０１）．其ＭＳＬＶ经钠－钙交换蛋白的钙摄取则明显降低（Ｐ＜０．０１或０．０５）：二．ＡＤＭ组的ＭＡＰ和ＬＶＩ则分别较ＬＮＮＡ组降低１９．６％和１１．３％，而其ＭＳＬＶ的钙摄取则高于ＬＮＮＡ组（Ｐ＜０．０５）；三、对照组、ＬＮＮＡ组和ＡＤＭ组钠－钙交换蛋白摄取钙的Ｋｍ值分别为７．５１．７．０４和７．５７ｕＭ，而Ｖｍａｘ则分别为６．３８，４．３２和５．４５ｎｍｏｌ／。ｍｇｐｒ／ｍｉｎ。表明：ＡＤＭ能拮抗ＬＮＮＡ诱导的高血压心肌肥大和减轻其ＭＳｌｌＶ钠－钙交换功能的损伤，并且后者可能是ＡＤＭ拮抗心肌肥大的机制之一。揭示内源性ＡＤＭ的诱导和外源性给予ＡＤＭ可能有预防和／或延缓高血压心肌肥大发生发展的作用。

The effects and mechanism of ADM on cardiac hypertrophy inLNNA-induced hypertensive and cardiac hypertrophic rats

The purpose of this to investigate the effects of adrenomedullin(ADM) on cardiac hypertrophy andthe loss of myocardial sarcolemmal vesicles (MSLV) Na-Ca exchanger in LNNA(via chronic nitric oxideblockade)-induced hypertensive and cardiac hypertrophic rats. The results show that :the mean arterialpressure (MAP) and left ventricular index(LVI) of LNNA group have increased by 57.4%and 18.0% respectivelyover that of the control(P<0.01), but its MSLV calcium uptake is lower than the control(p<0.01 or 0.01); 2 theMAP and the LVI of ADM group have decreased to 80.4% and 88.7% of the LNNA(P<0.01), its calcium uptakerate of MSLV is higer than the LNNA (P<0.05); 2, the difference of Km of MSLV Na-Ca exchanger amongcontrol, LNNA and and ADM groups is not obvious (7,51,7,04 and 7,57uM respectively), while the difference of theirVmax is great :6.38,4,32 and 5,45nmol/mg pr/min respectively. These results suggest that ADM has antagonism tocardiac hypertropy and that ADM can alleviate the loss of MSLV Na-CA exchanger induced by LNNA and toeffect of ADM may be one of the mechanisms of ADM to antagonize cardiac gypertreophy.