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Effects of lithium on angiotensin‐stimulated phosphatidylinositol turnover and aldosterone production in adrenal glomerulosa cells: a possible causal relationship
Author(s) -
Balla T.,
Enyedi P.,
Hunyady L.,
Spät A.
Publication year - 1984
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(84)80483-4
Subject(s) - aldosterone , medicine , endocrinology , phosphatidylinositol , angiotensin ii , phosphatidic acid , chemistry , zona glomerulosa , adrenal cortex , renin–angiotensin system , pi , biology , biochemistry , phospholipid , receptor , signal transduction , membrane , blood pressure
Turnover of 32 P‐labelled phosphatidylinositol (PI) was examined in isolated adrenal glomerulosa cells. Increased incorporation of [ 32 P] phosphate into PI in response to angiotensin II was completely prevented by Li + . A simultaneous accumulation of 32 P activity in phosphatidic acid (PA) was also observed. Angiotensin II increased the breakdown of PI despite the presence of Li + . These results suggest that Li is a suitable tool to interrupt the accelerated PI cycle in angiotensin‐stimulated cells. Aldosterone production of superfused cells was inhibited by Li + when the cells were stimulated with angiotensin II. On the other hand, Li + did not inhibit the aldosterone response of the cells to ACTH, a hormone which acts via cyclic AMP and does not enhance PI turnover in these cells. On the basis of these results, we assume that the inhibitory effect of Li + on aldosterone production is related to its effect on PI turnover.