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Adrenoceptors in SHR: alterations in binding characteristics and intracellular signal transduction pathways.

机译:SHR中的肾上腺素受体:结合特征和细胞内信号转导途径的改变。

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摘要

There is much data on altered adrenoceptor function in the heart, blood vessel and kidney from spontaneously hypertensive rats (SHR). The enhancement of vascular and renal alpha-adrenoceptor function, i.e. vasoconstriction and retention of water and sodium, may contribute to the development and maintenance of the hypertension, whereas cardiac alpha1-adrenoceptor may be of minor physiological significance. Alpha1-adrenoceptor-mediated signal transduction as a whole is increased in SHR vascular tissues, but the intracellular signaling per receptor in the kidney seems to be decreased despite increased alpha1-adrenoceptor density. On the other hand, cardiac and vascular beta-adrenoceptor responsiveness is attenuated in SHR. Reduced vasorelaxation mediated by beta-adrenoceptors may also contribute to high blood pressure. The impaired cardiovascular beta-adrenoceptor function in SHR does not appear to be necessarily explained by alterations observed at receptor levels. Alterations in signal transduction should be also considered. Limited data on renal beta-adrenoceptor density and its signaling suggest decreased or unaltered cyclic AMP formation per receptor in SHR. We will review alterations in both binding characteristics and each component of intracellular signal transduction pathways in cardiovascular and renal adrenoceptors of SHR.
机译:关于自发性高血压大鼠(SHR)的心脏,血管和肾脏中肾上腺素受体功能改变的大量数据。血管和肾脏α-肾上腺素受体功能的增强,即血管收缩和水和钠的滞留,可能有助于高血压的发展和维持,而心脏α1-肾上腺素受体可能具有较小的生理意义。整体而言,SHR血管组织中Alpha1-肾上腺素受体介导的信号转导增加,但是尽管α1-肾上腺素受体密度增加,但肾脏中每个受体的细胞内信号传导似乎减少。另一方面,心脏和血管β-肾上腺素受体反应性在SHR中减弱。 β-肾上腺素受体介导的血管舒张减少也可能导致高血压。 SHR的心血管β-肾上腺素受体功能受损似乎并不能通过在受体水平观察到的改变来解释。还应考虑信号传导的变化。关于肾脏β-肾上腺素受体密度及其信号传导的有限数据表明,SHR中每个受体的环状AMP形成减少或未改变。我们将审查SHR的心血管和肾脏肾上腺素能受体的结合特征和细胞内信号转导途径的每个组成部分的变化。

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