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血管紧张素刺激大鼠垂体前叶细胞培养物中β-内啡肽的释放。

Angiotensin stimulates beta-endorphin release from anterior pituitary gland cell cultures of rats.

作者信息

Kraft K, Lang R R, Gaida W, Unger T, Ganten D

出版信息

Neurosci Lett. 1984 Apr 20;46(1):25-9. doi: 10.1016/0304-3940(84)90193-9.

Abstract

The effect of exogenous and locally generated angiotensin II (ANG II) on the release of beta-endorphin (beta-END) from anterior pituitary cell cultures of rats was studied. Angiotensin I (ANG I) and ANG II stimulated the release of beta-END, the ANG I effects being inhibited by addition of the converting enzyme inhibitor captopril. Renin and angiotensinogen had no effect when given separately, but their combination increased beta-END release. Thus ANG II causes the release of beta-END, but the putative pituitary renin system cannot be stimulated by exogenous renin or angiotensinogen; converting enzyme, however, acts locally to produce biologically active ANG II from ANG I.

摘要

研究了外源性和局部产生的血管紧张素II(ANG II)对大鼠垂体前叶细胞培养物中β-内啡肽(β-END)释放的影响。血管紧张素I(ANG I)和ANG II刺激了β-END的释放,加入转化酶抑制剂卡托普利可抑制ANG I的作用。单独给予肾素和血管紧张素原没有作用,但它们联合使用可增加β-END的释放。因此,ANG II可导致β-END的释放,但外源性肾素或血管紧张素原不能刺激假定的垂体肾素系统;然而,转化酶可在局部作用,从ANG I产生具有生物活性的ANG II。

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