Abstract：
:We have previously shown that arginine vasopressin (AVP) stimulates the production of aldosterone in isolated superfused adrenal glomerulosa cells by a mechanism that involves an increased turnover of phosphoinositides. In the present study we compared the characteristics of AVP- and angiotensin II (AII)-induced changes in phosphoinositide turnover and aldosterone production in the rat. Selected concentrations of the two peptides, which were equipotent in terms of the magnitude of changes induced in phosphoinositide turnover, stimulated aldosterone production to the same extent only in the initial phase of the stimulation. A sustained aldosterone response was only observed in AII-stimulated cells. On the other hand, the AVP-induced increase in incorporation of [32P]phosphate into phosphatidylinositol and the stimulation of inositol phosphate production were maintained during incubation. Preincubation of the cells with AVP failed to modify the effects of AII on phosphoinositide breakdown or aldosterone production. These results indicate that desensitization at the level of the receptor or at a post-receptor site is not responsible for the transient character of AVP-induced aldosterone production. Delayed activation of an inhibitory mechanism by AVP can also be excluded. Additivity of the stimulation of the phosphoinositide turnover observed at submaximally, but not maximally, effective concentrations of AII indicates that the two agonists act on the same phosphoinositide pool. We suggest that the sustained steroidogenic effect of AII involves an as yet unidentified mechanism, which is absent when the cells are stimulated with AVP.
journal_name
J Mol Endocrinoljournal_title
Journal of molecular endocrinologyauthors
Enyedi P,Balla T,Antoni FA,Spät Adoi
10.1677/jme.0.0010117subject
Has Abstractpub_date
1988-09-01 00:00:00pages
117-24issue
2eissn
0952-5041issn
1479-6813journal_volume
1pub_type
杂志文章abstract：:Relaxin is a peptide hormone which is produced in human reproductive tissues including the ovary and prostate gland. Little is known of the molecular events regulating relaxin gene transcription. We have studied this question using gene transfer of relaxin promoter/reporter gene constructs into a relaxin-expressing ce...
journal_title：Journal of molecular endocrinology
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journal_title：Journal of molecular endocrinology
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journal_title：Journal of molecular endocrinology
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
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更新日期：2007-06-01 00:00:00
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更新日期：2002-10-01 00:00:00
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journal_title：Journal of molecular endocrinology
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journal_title：Journal of molecular endocrinology
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
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更新日期：2009-12-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
doi：10.1677/jme.0.0190183
更新日期：1997-10-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
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更新日期：2009-04-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
doi：10.1677/jme.0.0210291
更新日期：1998-12-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
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更新日期：2017-10-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
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更新日期：2010-01-01 00:00:00
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journal_title：Journal of molecular endocrinology
pub_type： 杂志文章
doi：10.1677/jme.0.0100115
更新日期：1993-04-01 00:00:00
