Stress－Indused Hypothermia Involves Stimulation of Adenosine A1－Receptors in Rats

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Subcutaneous (s.c.) injection of adenosine produced hyperthermia in non-stressed rats and potentiated hypotermia in stressed rats. The potent adenosine A1-recepter stimulants, N6-cyclohexyl adenosine (CHA) and N6-(L-phenylisopropyl) adenosine (L-PIA) prodused hypothermia even in non-stressed rats, which was markedly potentiated in stressed trats. Futhermore, intracerbral ventricular (I.c.v.) injection of adenosine or adenosine analogues produced potentiation of stress-induced hypotermia relative to that induced with s.c.injection. N6-(D-phenylisoprophyl) adenosine (D-PIA) did not affect core temperature. When rats were treated with adenosine 1 h before atress, and then exposed to stress, the hyperthemia exhibited in the non-stressed state changed to hypothermia in the stressed state. When the rats which were treated with adenosine and then atressed for 1 h were released from stress, the hypothermia observed in the atressed state progressively changed to hyperthemia. Low doses of β-endorphin (I.c.v.) and morphine (s.c.)reversed stress-induced hypothermia which was potentiated by CHA, although high doses of β-endorphin (I.c.v.) and morphine (s.c.) potentiated the stress-induced hypothermia. These results suggest that the effects of adenosine on core temperature in rats are altered depending upon the state of animals. Stress-induced hypothermia may be, at least in part, mediated by endogenous adenosine which seems to selectively activate A1-receptor in the stressed state.

Stress－Indused Hypothermia Involves Stimulation of Adenosine A1－Receptors in Rats

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