title: Oestrogenic influence on brain AT1 receptor signalling on the thirst and sodium appetite in osmotically stimulated and sodium-depleted female rats.
abstract: The present work was carried out to investigate the role of angiotensin II type 1 (AT(1)) receptors in nocturnal thirst and sodium appetite induced by classical models of osmotic and sodium depletion challenges in ovariectomized rats chronically treated with oil or oestradiol benzoate (EB, 20 microg per animal, s.c. daily). In both conditions, the animals were given saline or losartan (108 nmol per animal, i.c.v.), a selective AT(1) receptor blocker. Oestrogen therapy significantly reduced the water intake induced by water deprivation, sodium depletion produced by frusemide injected 24 h before, and s.c. acute frusemide plus captopril injection (FUROCAP protocol), with no alteration following s.c. hypertonic saline injection. In contrast, EB therapy decreased the salt intake induced by sodium depletion and FUROCAP protocols, with no alteration following water deprivation and s.c. hypertonic saline injection. Central AT(1) blockade inhibited the dipsogenic response induced by water deprivation, osmotic stimulation, chronic sodium depletion and FUROCAP protocols and inhibited the natriorexigenic response induced by sodium depletion in ovariectomized rats. Oestrogen therapy significantly attenuated the losartan-induced antidipsogenic and antinatriorexigenic actions following sodium depletion and FUROCAP protocols. These results indicate that ovariectomized rats express increased AT(1) receptor signalling related to thirst and sodium appetite responses. Oestrogen therapy and brain AT(1) receptor blockade weakened or markedly decreased the behavioural responses during the nocturnal period, a time at which brain angiotensinergic activity is expected to be more prominent. Finally, we demonstrated through different experimental protocols a clear-cut influence of oestrogenic status on the behavioural AT(1)-induced signalling response.
authors.affiliation: Department of Physiological Sciences, Biology Institute, Federal Rural University of Rio de Janeiro, BR465, Km 7, 23890-000, Seropédica, RJ, Brazil.
authors.forename: A S
authors.initials: AS
authors.lastname: Mecawi
authors.forename: A
authors.initials: A
authors.lastname: Lepletier
authors.forename: I G
authors.initials: IG
authors.lastname: Araujo
authors.forename: F V
authors.initials: FV
authors.lastname: Fonseca
authors.forename: L C
authors.initials: LC
authors.lastname: Reis
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002216:Captopril / Q000494:pharmacology; D003270:Contraceptive Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004232:Diuretics / Q000494:pharmacology; D004326:Drinking / Q000187:drug effects* / Q000502:physiology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D007010:Hyponatremia / Q000503:physiopathology*; D019808:Losartan / Q000494:pharmacology; D010052:Ovariectomy; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D013894:Thirst / Q000187:drug effects* / Q000502:physiology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D003270:Contraceptive Agents; D004232:Diuretics; D004967:Estrogens; D044140:Receptor, Angiotensin, Type 1; C074283:estradiol 3-benzoate; D004958:Estradiol; D005665:Furosemide; D002216:Captopril; D019808:Losartan