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高血压中调节心肌肥厚的因素。

Factors regulating myocardial hypertrophy in hypertension.

作者信息

Sen S

出版信息

Circulation. 1987 Jan;75(1 Pt 2):I81-4.

PMID:2947754
Abstract

Evidence for the existence of factor(s) other than blood pressure responsible for modulation of myocardial hypertrophy accompanying hypertension is well documented. A factor that has been isolated from the myocardium of the spontaneously hypertensive rat and partially purified has been shown to stimulate protein synthesis in vitro. Three indexes of protein synthesis, namely incorporation of 3H-leucine into myocyte myosin, specific activity of the leucyl tRNA, and rate of protein synthesis, also were observed to significantly increase on exposure to this factor, which may play a key role in the modulation of myocardial hypertrophy that accompanies hypertension. Evidence has also been presented demonstrating the role of unknown factors that control the shift of myosin isozymes from V1 (a high-ATPase, high-contractile protein type) to V3 (a slow ATPase type myosin), and vice versa. This study demonstrates that the modulation of the myocardial mass can be controlled at different levels: first at an intrinsic intracellular level by the mechanism of a local growth factor, and then at the level of the contractile protein, the quality rather than quantity of which was found to be important. Both of these were observed to be modulated by factor(s) independent of blood pressure and myocardial mass. However, it remains to be determined what is responsible at the genetic level for transmitting the signal that selects what type of protein will be synthesized and whether there is a common pathway among all the controlling factors.

摘要

有充分文献证明,除血压外,还存在其他因素可调节高血压伴发的心肌肥大。从自发性高血压大鼠心肌中分离并部分纯化的一种因子,已被证明在体外可刺激蛋白质合成。在接触该因子时,蛋白质合成的三个指标,即3H-亮氨酸掺入心肌肌球蛋白、亮氨酰tRNA的比活性和蛋白质合成速率,也均显著增加,该因子可能在调节高血压伴发的心肌肥大中起关键作用。也有证据表明存在未知因子,它们控制着肌球蛋白同工酶从V1(一种高ATP酶、高收缩蛋白类型)向V3(一种慢ATP酶型肌球蛋白)的转变,反之亦然。本研究表明,心肌质量的调节可在不同水平进行:首先在内在细胞内水平通过局部生长因子机制进行,然后在收缩蛋白水平进行,发现收缩蛋白的质量而非数量很重要。这两者均被发现受独立于血压和心肌质量的因子调节。然而,在基因水平上,是什么负责传递选择合成何种类型蛋白质的信号,以及所有控制因子之间是否存在共同途径,仍有待确定。

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