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人类醛固酮瘤中缺乏心房利钠肽受体。

Lack of atrial natriuretic peptide receptors in human aldosteronoma.

作者信息

Shionoiri H, Hirawa N, Takasaki I, Ishikawa Y, Oda H, Gotoh E, Hosaka M, Shimonaka M, Ishido M, Hirose S

机构信息

Second Department of Internal Medicine, Yokohama City University, Japan.

出版信息

Biochem Biophys Res Commun. 1988 Apr 15;152(1):37-43. doi: 10.1016/s0006-291x(88)80676-4.

DOI:10.1016/s0006-291x(88)80676-4
PMID:2833892
Abstract

The effect of synthetic alpha-human atrial natriuretic peptide (ANP) on aldosterone secretion was studied in human aldosterone producing adrenocortical adenoma obtained surgically from a patient with primary aldosteronism and in human apparently normal adjacent adrenal cortical tissues obtained from a patient with pheochromocytoma, in vitro. Apparently normal adrenal cortical tissue responded to ANP with the known inhibition of aldosterone secretion. In contrast, the aldosterone producing adenoma did not respond to ANP. When stimulated by either ACTH or angiotensin II, there is no inhibition by ANP in the adenoma tissue, whereas normal tissue was inhibited. Immunohistochemical examination utilizing an ANP-receptor antiserum demonstrated that there was no evidence of binding site in the cortical adenoma, in contrast, zona glomerulosa cells in the cortical tissues adjacent to either aldosterone producing adenoma or pheochromocytoma were densely stained. This apparent lack of ANP-receptors is an associated finding with the hypersecretion of aldosterone in the aldosterone producing adenoma.

摘要

在体外,研究了合成的α-人心房利钠肽(ANP)对从原发性醛固酮增多症患者手术切除的产生醛固酮的肾上腺皮质腺瘤以及从嗜铬细胞瘤患者获取的明显正常的相邻肾上腺皮质组织中醛固酮分泌的影响。明显正常的肾上腺皮质组织对ANP有反应,表现为已知的醛固酮分泌受抑制。相反,产生醛固酮的腺瘤对ANP无反应。当受到促肾上腺皮质激素(ACTH)或血管紧张素II刺激时,腺瘤组织中ANP无抑制作用,而正常组织受到抑制。利用ANP受体抗血清进行的免疫组织化学检查表明,皮质腺瘤中没有结合位点的证据,相反,与产生醛固酮的腺瘤或嗜铬细胞瘤相邻的皮质组织中的球状带细胞被密集染色。这种明显缺乏ANP受体的情况与产生醛固酮的腺瘤中醛固酮分泌过多相关。

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Lack of atrial natriuretic peptide receptors in human aldosteronoma.人类醛固酮瘤中缺乏心房利钠肽受体。
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引用本文的文献

1
Natriuretic peptides receptors in human aldosterone-secreting adenomas.人醛固酮分泌性腺瘤中的利钠肽受体
J Endocrinol Invest. 1999 Jul-Aug;22(7):514-8. doi: 10.1007/BF03343602.