Glucocorticoids potentiate the dipsogenic action of angiotensin II.

The effect of a short-term, acute treatment with a glucocorticoid, dexamethasone sodium phosphate, on the drinking induced by angiotensin II (AII) was investigated in a series of experiments. Initial studies indicated that a single injection of dexamethasone (700-750 micrograms/kg, i.p.) reduced food intake, body weight and water intake for up to 48 h, but had little effect on blood pressure when it was measured 6 h subsequent to the injection. The drinking elicited by peripherally administered AII (200 micrograms/kg, s.c.) was enhanced if the glucocorticoid (700 micrograms/kg, i.p.) was given 3 h or 6 h prior to the dipsogen. There was no effect of pretreatment with the steroid if the drinking test was delayed by 24 h. The subsequent experiment showed that the glucocorticoid effect on AII-stimulated drinking was dose dependent (100 micrograms-1600 micrograms/kg). The drinking stimulated by intracerebroventricular (i.c.v.) AII (2.5 ng) was enhanced in terms of volume and total duration by prior treatment with dexamethasone, but i.c.v. carbachol (200 ng)-induced drinking remained unaffected. The final study showed that binding of AII to its receptors in five different areas of the rat brain was not affected by prior treatment with dexamethasone.