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Angiotensin-II (A-II) provoked a rapid decrease in 32p in triphosphoinositide (TPI) in 32p-prelabeled rat adrenal glomerulosa cells. This effect (presumably reflecting TPI hydrolysis) of A-II was nearly maximal at 5 sec of incubation and appeared to precede increases in labeling of phosphatidic acid and phosphatidylinositol. 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-II action in glomerulosa tissue.
Farese et al. (Sun,) studied this question.
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