Why the study?
Does Angiotensin-II affect polyphosphoinositide metabolism in rat adrenal glomerulosa cells?
Does Angiotensin-II affect polyphosphoinositide metabolism in rat adrenal glomerulosa cells?
Angiotensin-II induces rapid triphosphoinositide hydrolysis in rat adrenal glomerulosa cells, suggesting a potential mechanism for calcium mobilization during its action.
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Hypothesis-generating for Ang-II calcium signaling via TPI in glomerulosa cells; leaves open human relevance.
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.
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Farese et al. (1984) studied this question.
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