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Absence of angiotensin II type 1 receptor gene mutations in human adrenal tumors.

Abstract：

:Regulatory actions of angiotensin II (AngII), which is involved in the pathophysiology of hypertension and also participates in cell proliferation and cell differentiation, are mainly mediated by AngII type 1 (AT1) receptor. Recently, activating mutations of receptors causing hyperfunctioning endocrine diseases have been described in the case of the TSH and LH receptors, implicating that such mutations might occur in other G-protein-coupled receptors. Furthermore it seems to be possible that genetic variations of AT1 receptor have an influence upon the action of AngII. Therefore, we searched by sequence analysis of the coding region of AT1 receptor gene for activating mutations and genetic polymorphisms in 56 human adrenal tumors (16 aldosterone-producing adenomas, 10 cortisol-producing adenomas, 1 aldosterone-producing carcinoma, and 29 incidentalomas). We were not able to identify any activating mutation in the coding region of AT1 receptor gene. We conclude that activating mutations of the AT1 receptor are not a major cause of the development of adrenal adenomas, if at all. In addition, polymorphic subtypes of AT1 receptor do not seem to play a major role in the pathogenesis of these tumors, even though a tendency towards a higher frequency of the polymorphic base substitution at position 573 (T573-->C) in cortisol-producing tumors needs to be further evaluated.

journal_name

Eur J Endocrinol

journal_title

European journal of endocrinology

authors

Sachse R,Shao XJ,Rico A,Finckh U,Rolfs A,Reincke M,Hensen J

doi

10.1530/eje.0.1370262

subject

Has Abstract

pub_date

1997-09-01 00:00:00

pages

262-6

issue

3

eissn

0804-4643

issn

1479-683X

journal_volume

137

pub_type

杂志文章

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