Rapid effects of angiotensin-i I on polyphosphoinositide metabolism in the rat adrenal glomerulosa

Robert V. Farese, Ronald E. Larson, John S. Davis

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Abstract

Angiotensin-1 I (A-ll) provoked a rapid decrease in 32p jn triphosphoinositide (TPI) in 32p-pre-labeled rat adrenal glomerulosa cells. This effect (presumably reflecting TPI hydrolysis) of A-ll was nearly maximal at 5 sec of incubation and appeared to precede increases in labeling of phosphatidic acid and phosphat idylinositol. Other aldosterone-stimulating agents (ACTH, K+ and serotonin) did not provoke this effect. Since this effect appeared to be independent of Ca++, it is possible that TPI hydrolysis may be important for Ca ++ mobilization during A-ll action in glomerulosa tissue.

Original languageEnglish (US)
Pages (from-to)302-304
Number of pages3
JournalEndocrinology
Volume114
Issue number1
DOIs
StatePublished - Jan 1 1984

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Zona Glomerulosa
Phosphatidylinositol Phosphates
Angiotensin I
Hydrolysis
Phosphatidic Acids
Aldosterone
Adrenocorticotropic Hormone
Serotonin
triphosphoinositide

ASJC Scopus subject areas

  • Endocrinology

Cite this

Rapid effects of angiotensin-i I on polyphosphoinositide metabolism in the rat adrenal glomerulosa. / Farese, Robert V.; Larson, Ronald E.; Davis, John S.

In: Endocrinology, Vol. 114, No. 1, 01.01.1984, p. 302-304.

Research output: Contribution to journalArticle

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