The hypothermic effect of clonidine and other imidazolidines in relation to their ability to enter the central nervous system in mice.
Clonidine and several other structurally related imidazolidines were administered intraperitoneally to mice and their capacity to cause hypothermia was used as an indication of their ability to enter the central nervous system. The substances were: clonidine (2-[w,6 dichlorophenylimino] imidazolidine) and its 2, 6-disubstituted derivates: St 91 (2,6-diethyl), St 93 (2-chloro, 6-methyl), St 95 (2,6-dimethyl) and St 1697 (2-ethyl, 6-methyl). All caused dose-dependent reductions in body temperature. Clonidine was most potent and was effective over the range 62.5-500 millimicron/kg i.p. clonidine lowered body temperature by 2.9 0.15oC. Relative potencies (R) were: clonidine (R 1), St 91 (0.41), St 1697 (0.29), St 93 (0.21) and St 95 (0.06). Hypothermia was inhibited by piperoxan injected intracisternally (10 millimicron/kg) but not intraperitoneally (10 and 50 millimicron/kg). Following intracisternal administration, the imidazolidine dose response curves were shifted in a parallel fashion to the left relative to the intraperitoneal administration. It is suggested that these compounds can all cross the blood-brain barrier in mice and interact with central alpha-adrenoceptors to cause hypothermia. These findings are at variance with the abilities of some of these substances to cause sedation and hypotension mediated by interaction with central alpha-adrenoceptors.[1]References
- The hypothermic effect of clonidine and other imidazolidines in relation to their ability to enter the central nervous system in mice. McLennan, P.L. Eur. J. Pharmacol. (1981) [Pubmed]
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