Effect of sodium intake on phosphoinositides and inositol trisphosphate response to angiotensin II, K+ and ACTH in rat glomerulosa cells

Abstract

ABSTRACT 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 (2×105 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)+inositol3) + 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 pmoler incubate respectively, indistinguishable from those observed in rats on a normal Na+ intake, except for the significantly (P<0·025) greater Ptdlns 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 had 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. In addition, PtdIns 4,5-P2 did not return to control levels in cells obtained from animals on a low sodium intake. However, the most striking differences were observed in response to ACTH. In animals maintained on a normal sodium intake, there were no changes in any of the four compounds. In contrast, there was a sharp increase in all four substances in response to ACTH when the cells were obtained from animals on a low sodium intake, with peak levels occurring at 8 s, similar to that observed with potassium. Thus, changes in the response pattern of the phosphoinositides may mediate the altered adrenal responsiveness to AII and ACTH with sodium restriction. Journal of Endocrinology (1989) 122, 371–377