Abstract：
:Earlier studies showed that pretreatment (3 and 6 h) of rats with the glucocorticoid hormone, dexamethasone, potentiated the drinking response to either central or peripheral administration of angiotensin II (AII). In the present study the specificity and mechanisms of this potentiation were examined. Intraperitoneal (i.p.) injection of rats with the pure glucocorticoid agonist, RU 28362 (0.4-1.6 mg/kg; 3-24 h), resulted in a time- and dose-dependent potentiation of the drinking responses to either peripherally (100 micrograms/kg, s.c.) or centrally (10 ng) injected AII, similar to the effects of dexamethasone. Drinking induced by central injection of carbachol (200 ng) was unaltered by pretreatment with RU 28362, suggesting that potentiation by this compound was specific for AII. The potentiation of AII-induced drinking by either dexamethasone or RU 28362 was completely abolished by pretreatment with the glucocorticoid Type II receptor (GR) antagonist, RU 38486 (2 mg/kg, i.p.), but not by the mineralocorticoid Type I receptor (MR) blocker, mespirenone (2 mg/kg, i.p.). Taken together, these results indicate that the glucocorticoid-induced potentiation of AII-induced drinking is mediated via GR. Associated with the fact that glucocorticoids potentiate AII-induced drinking is the observation that these steroids also potentiate AII-induced urine output. This enhancement of urine output may explain in part the potentiation in drinking behavior. Possible mechanisms are discussed.
journal_name
Brain Resjournal_title
Brain researchauthors
Sumners C,Gault TR,Fregly MJdoi
10.1016/0006-8993(91)90093-bsubject
Has Abstractpub_date
1991-06-28 00:00:00pages
283-90issue
2eissn
0006-8993issn
1872-6240pii
0006-8993(91)90093-Bjournal_volume
552pub_type
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