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心房利钠肽(ANP)作为一种神经肽:在容量控制和肾脏钠处理方面与血管紧张素II的相互作用。

Atrial natriuretic peptide (ANP) as a neuropeptide: interaction with angiotensin II on volume control and renal sodium handling.

作者信息

Unger T, Badoer E, Gareis C, Girchev R, Kotrba M, Qadri F, Rettig R, Rohmeiss P

机构信息

Department of Pharmacology, University of Heidelberg, FRG.

出版信息

Br J Clin Pharmacol. 1990;30 Suppl 1(Suppl 1):83S-88S. doi: 10.1111/j.1365-2125.1990.tb05473.x.

Abstract
  1. Angiotensin II (ANG II) and atrial natriuretic peptide (ANP) are functionally antagonistic circulating hormones involved in blood pressure and body fluid regulation. An inappropriate atrial secretion of ANP has been implicated in the pathogenesis of hypertension, but clinical and experimental results on the role of ANP in hypertension are still conflicting. 2. In the brain both peptides have been localized in close proximity, preferentially in areas involved in central cardiovascular, electrolyte and volume control. ANP was shown to inhibit ANG II-induced drinking, release of pituitary hormones and natriuresis, and to induce sodium retention when given alone. 3. These findings suggest that also in the brain ANG II and ANP exert functionally antagonistic effects. However, in contrast to their peripheral effects, ANG II induces natriuresis while ANP appears to cause antinatriuresis in the brain.
摘要
  1. 血管紧张素II(ANG II)和心房利钠肽(ANP)是参与血压和体液调节的功能拮抗循环激素。心房利钠肽分泌不当与高血压发病机制有关,但关于心房利钠肽在高血压中作用的临床和实验结果仍相互矛盾。2. 在大脑中,这两种肽定位相近,优先存在于参与中枢心血管、电解质和容量控制的区域。研究表明,心房利钠肽可抑制血管紧张素II诱导的饮水、垂体激素释放和利钠作用,单独给药时可诱导钠潴留。3. 这些发现表明,在大脑中血管紧张素II和心房利钠肽也发挥功能拮抗作用。然而,与它们的外周作用相反,血管紧张素II在大脑中诱导利钠作用,而心房利钠肽似乎导致钠潴留。

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