Role of nitric oxide in systemic vasopressin-induced hypothermia

Abstract

It has been reported that arginine vasopressin (AVP) plays a thermoregulatory action, but very little is known about the mechanisms involved. In the present study, we tested the hypothesis that nitric oxide (NO) plays a role in systemic AVP-induced hypothermia. Rectal temperature was measured before and after AVP, AVP blocker, or N(G)-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature (T(b)) measured in control animals was 36.53 ± 0.08°C. We observed a significant (P < 0.05) reduction in T(b) to 35.44 ± 0.19°C after intravenous injection of AVP (2 μg/kg) and to 35.74 ± 0.10°C after intravenous injection of L- NAME (30 mg/kg). The systemic injection of the AVP blocker [β-mercapto- β,β-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin (10 μg/kg) caused a significant increase in T(b) to 37.33 ± 0.23°C, indicating that AVP plays a tonic role by reducing T(b). When the treatments with AVP and L-NAME were combined, systemically injected L-NAME blunted AVP-induced hypothermia. To assess the role of central thermoregulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected into the third cerebral ventricle. Intracerebroventricular injection of L-NAME caused an increase in T(b), but when intracerebroventricular L-NAME was combined with systemic AVP injection (2 μg/kg), no change in T(b) was observed. The data indicate that central NO plays a major role mediating systemic AVP-induced hypothermia.