CHRONIC LOSARTAN TREATMENT BLOCKS ISOPROTERENOL-INDUCED DIPSOGENESIS

Previous studies suggest that beta-adrenergic receptor agonists and ot her hypotensive agents stimulate water intake via the renin-angiotensi n system (RAS). However, a recent study reported that acute peripheral administration of Losartan, an angiotensin II (AII) type I receptor a ntagonist, failed to inhibit isoproterenol-induced water intake. In th e current study we assessed the role of chronic Losartan treatment on isoproterenol-induced water intake. Male Sprague-Dawley rats were divi ded into two groups (n = 10/group). The experimental group was chronic ally treated with Losartan in the drinking water (120 mg/kg/day). Rats in the control group were maintained on normal tap water. At the end of each week, water intake in response to isoproterenol was determined . On the days of the dipsogenic study, water intake was determined 1 h prior to and 2 h following SC injection of isoproterenol (25 mu g/kg) . Isoproterenol-induced water intake in the experimental group was sig nificantly lower than the control rats by 71% and 88% at the end of we eks one and two respectively (p < 0.01). Following an days of Losartan treatment, dipsogenic response to AII likewise demonstrated a complet e blockage of AII receptors (75% decrease compared to the controls). T hese data strongly suggest that water intake in response to isoprotere nol is mediated in part by the RAS.