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 language | English (US) |
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Pages (from-to) | 302-304 |
Number of pages | 3 |
Journal | Endocrinology |
Volume | 114 |
Issue number | 1 |
DOIs | |
State | Published - 1984 |
Externally published | Yes |
ASJC Scopus subject areas
- Endocrinology