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垂体前叶调节心房利钠肽从心脏心房的释放。

Anterior pituitary gland modulates the release of atrial natriuretic peptides from cardiac atria.

作者信息

Zamir N, Haass M, Dave J R, Zukowska-Grojec Z

出版信息

Proc Natl Acad Sci U S A. 1987 Jan;84(2):541-5. doi: 10.1073/pnas.84.2.541.

Abstract

Myocytes in the atria contain a prohormone that gives rise to atrial natriuretic peptides (ANP), which have intrinsic hemodynamic regulatory activity. Little is known about mechanisms regulating ANP release. In rats with indwelling catheters, acute blood volume expansion with 5% (wt/vol) dextrose increases the amount of circulating immunoreactive ANP by a factor of 2-3, as determined by radioimmunoassay. Pithing, which both removes neurogenic influences and interrupts humoral influences of the brain and pituitary gland on the heart, completely blocked stimulus-induced release of ANP. Because our studies using pharmacological blockade of the autonomic nervous system had suggested that neurogenic mechanisms do not play a major role in ANP release, we sought a humoral mechanism involved in ANP secretion. Basal and stimulated release of ANP were significantly blunted in hypophysectomized rats (8 days after operation) but were completely restored when the resected anterior pituitary was reimplanted under the kidney capsule. This suggests that hormones of anterior pituitary origin are required for ANP secretion in response to acute volume loading.

摘要

心房中的心肌细胞含有一种前激素,可产生具有内在血流动力学调节活性的心房利钠肽(ANP)。关于调节ANP释放的机制知之甚少。在留置导管的大鼠中,通过放射免疫测定法测定,用5%(重量/体积)葡萄糖进行急性血容量扩张可使循环中免疫反应性ANP的量增加2至3倍。毁髓术可消除神经源性影响,并中断大脑和垂体对心脏的体液影响,它完全阻断了刺激诱导的ANP释放。因为我们使用自主神经系统药理学阻断的研究表明,神经源性机制在ANP释放中不发挥主要作用,所以我们寻找一种参与ANP分泌的体液机制。在垂体切除的大鼠(术后8天)中,ANP的基础释放和刺激释放显著减弱,但当切除的垂体前叶重新植入肾包膜下时,释放完全恢复。这表明垂体前叶来源的激素是ANP对急性容量负荷作出分泌反应所必需的。

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