Spinal alpha-adrenoceptor and dynorphin involvement in the depressor effect of clonidine

Intrathecal injection (ith) of clonidine (1 μg) in rats caused a decrease in the mean blood pressure (-52±12mm Hg, ±SD) and heart rate (-99±24 beats/min) which were partly antagonized by ith α-adrenoceptor blocker phentolamine (30μg), or the selective α1 or α2-adrenoceptor blocker prazosin or yohimdine (30 μg, respectively). The effects of clonidine was also blocked by opiate antagonist naloxone (10 mg/kg, iv) or by pretreatment with dynorphin antiserum (10μl,ith). Naloxone (0.5 mg/kg, iv) or pretreatment with control serum (10 μl, ith) failed to reduce the effects of clonidine. The results suggest that an activation of α1 and α2-receptors and the release of dynorphin in spinal cord are important for mediating the depressor effect of ith clonidine.