Effects of lithium on angiotensin-stimulated phosphatidylinositol turnover and aldosterone production in adrenal glomerulosa cells: a possible causal relationship |
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Authors: | T Balla P Enyedi L Hunyady A Spät |
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Institution: | Department of Physiology, Semmelweis University Medical School, H-1444 Budapest, PO Box 259, Hungary |
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Abstract: | Turnover of 32P-labelled phosphatidylinositol (PI) was examined in isolated adrenal glomerulosa cells. Increased incorporation of 32P]phosphate into PI in response to angiotensin II was completely prevented by Li+. A simultaneous accumulation of 32P 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. |
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Keywords: | Phosphatidylinositol metabolism Lithium Aldosterone Angiotensin II Corticotropin PI phosphatidylinositol PA phosphatidic acid PS phosphatidylserine PE phosphatidylethanolamine PC phospatidlcholine ACTH adrenocorticotropin |
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