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首页> 外文期刊>Life sciences >Dysfunction of myocardial sarcoplasmic reticulum in rats with myocardial calcification.
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Dysfunction of myocardial sarcoplasmic reticulum in rats with myocardial calcification.

机译：心肌钙化大鼠心肌肌质网功能障碍。

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摘要

We investigated the relationship between cardiac dysfunction and Ca(2+) transport in the myocardial sarcoplasmic reticulum (SR) during the pathogenesis of cardiovascular calcification in rats. The possible mechanism of SR dysfunction was explored by detecting the alteration of the nitric oxideitric oxide synthase (NO/NOS) pathway in the SR. Using the vitamin D plus nicotine (VDN treatment for 2 week and 6 week) experimental model of cardiac calcification, cardiac function and sarcoplasmic reticulum function were measured. Inhibition of cardiac functions in vivo (peak rate of contraction and peak rate of relaxation, P<0.05 or P<0.01) were observed in all calcification groups, simultaneously, Ca(2+) release and uptake in the SR as well as the Ca(2+) release channel and Ca(2+) pump activity were inhibited. Myocardial Ca(2+) concentration and cardiac and SR dysfunction were inversely related (P<0.05). The specific NO/NOS pathway (NO production, NOS activity and nNOS expression in the SR) was upregulated in the SR and associated with calcification (both 2- and 6 week VDN groups). These results indicate that cardiac dysfunction associated with myocardial calcification might be mediated by SR dysfunction, which may result from an impaired SR-specific NO/NOS pathway.
机译：我们调查了大鼠心肌钙化的发病机理中，心脏功能障碍与心肌肌浆网（SR）中Ca（2+）转运之间的关系。通过检测SR中一氧化氮/一氧化氮合酶（NO / NOS）途径的改变，探索了SR功能障碍的可能机制。使用维生素D加尼古丁（VDN治疗2周和6周）测量心脏钙化，心脏功能和肌浆网功能的实验模型。在所有钙化组中均观察到体内心脏功能的抑制（收缩峰值速率和松弛峰值速率，P <0.05或P <0.01），同时，SR和Ca中的Ca（2+）释放和摄取（2+）释放通道和Ca（2+）泵活动受到抑制。心肌Ca（2+）浓度与心脏和SR功能障碍呈负相关（P <0.05）。特定的NO / NOS途径（SR中的NO产生，NOS活性和nNOS表达）在SR中上调并与钙化相关（VDN组为2周和6周）。这些结果表明，与心肌钙化相关的心脏功能障碍可能是由SR功能障碍介导的，这可能是由SR特异性NO / NOS途径受损引起的。

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