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.
ASJC Scopus subject areas