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  • Title: Clonidine antagonism of angiotensin-related drinking: a central site of action.
    Author: Fregly MJ, Rowland NE, Greenleaf JE.
    Journal: Brain Res; 1984 Apr 30; 298(2):321-7. PubMed ID: 6326953.
    Abstract:
    Administration of either isoproterenol (25 micrograms/kg, s.c.) or angiotensin II (200 micrograms/kg, s.c.) induces drinking in rats within 0.5-1 h. This drinking was inhibited by prior administration of the presynaptic alpha-adrenergic agonist clonidine (12 micrograms/kg, i.p.). Urine output was enhanced by clonidine in the angiotensin II-, but not the isoproterenol-treated group. Drinking in response to peripheral administration of either angiotensin II or isoproterenol was also inhibited by intracerebroventricular (i.v.t.) administration of clonidine (8 micrograms/kg). This dose of clonidine also enhanced the urine output after angiotensin II. Further, the drinking induced by i.v.t. administration of angiotensin II, at 4 but not 20 ng/kg was inhibited by peripheral administration of clonidine (12 micrograms/kg, i.p.). When clonidine was administered i.v.t. prior to i.v.t. injection of either angiotensin II (20 ng/kg) or carbachol (1.2 micrograms/kg), the drinking response to these dipsogens was attenuated. These results suggest that clonidine may act centrally to attenuate drinking at a site, possibly in the nucleus tractus solitarius, that may be considered a final common pathway for this response.
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