To assess the impact of sodium intake on the adrenal phosphoinositide system, rats were maintained on a low or normal salt diet for 5 days, and glomerulosa cell preparations (2 x 10(5) cells) were stimulated by angiotensin II (AII; 10 nmol/l), potassium (K+; 8.7 mmol/l) or ACTH (0.1 nmol/l) for 0, 2, 4, 6, 12, 15 and 60 s. Levels of phosphatidylinositol (PtdIns), phosphatidylinositol 4-phosphate (PtdIns 4-P), phosphatidylinositol 4,5-bisphosphate (PtdIns 4,5-P2) and inositol 1,4,5-trisphosphate (Ins 1,4,5-P3) + inositol 1,3,4-trisphosphate (Ins 1,3,4-P3) were assayed by a microspectrophotometric procedure. Non-stimulated levels of PtdIns, PtdIns 4-P, PtdIns 4,5-P2 and Ins 1,4,5-P3 (+ Ins 1,3,4-P3) (means +/- S.E.M.; n = 36) in cells from rats on the low Na+ intake were 580 +/- 6.5, 187 +/- 2.6, 82 +/- 3 and 95 +/- 1.2 pmol per incubate respectively, indistinguishable from those observed in rats on a normal Na+ intake, except for the significantly (P less than 0.025) greater PtdIns 4,5-P2 level. In response to AII stimulation, all four compounds showed an earlier and greater peak response when cells were obtained from animals on a low rather than a high sodium intake. All values has returned to control levels by 12-15 s, regardless of the level of sodium intake. In contrast, with K+ stimulation there were no differences in the peak response of cells from rats on the two dietary intakes, but there was a shift of the peak to a longer time-interval (6 versus 8 s) in animals maintained on a low sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)