CENTRAL ALPHA-2-ADRENOCEPTOR-MEDIATED PRESSOR-RESPONSE TO CLONIDINE IN CONSCIOUS, SPONTANEOUSLY HYPERTENSIVE RATS

Pressor responses to intracerebroventricular (i.c.v.) injection of clonidine were investigated in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Clonidine (1-10-mu-g, i.c.v.) caused a dose-dependent pressor response and decrease in heart rate in both SHR and WKY. In SHR, low doses (1, 2.5-mu-g) but not high doses (5, 10-mu-g) of i.c.v.-clonidine induced a depressor response following the pressor response. Both pressor and depressor responses to i.c.v.-clonidine were significantly greater in SHR than in WKY. In both SHR and WKY, pressor responses to i.c.v.-clonidine were abolished by pentobarbital anesthesia, pretreatment with i.v.furosemide (5 mg/kg), 24-hr water deprivation and pretreatment with i.c.v.-yohimbine (100-mu-g), but not by pretreatment with i.v.-yohimbine (100-mu-g) and i.c.v.-prazosin (10-mu-g). On the 1st day after surgery for arterial catheter implantation, SHR reduced their water intake, and i.c.v.-clonidine (5-mu-g) caused a slight pressor response, whereas the same dose of clonidine on the 7th day after surgery resulted in a marked pressor response. These results suggest that clonidine caused a central alpha-2-adrenoceptor-mediated pressor response, which is greater in SHR than in WKY and is sensitive to body fluid volume changes and anesthesia.