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AIM: To investigate the effect of peripheral administration of arginine vasopressin (AVP) on lipopolysaccharide (LPS)-induced fever and hyperalgesia in rats and its relationship with interleukine-1β (IL-1β) and prostaglandin E2 (PGE2).METHODS: The core temperature (Tc), brown adipose tissue (BAT) temperature and activity were measured by telemetry in adult male Sprague-Dawley rats at an ambient temperature of 23 ℃ during a 12 h light/12 h dark photoperiod (lights on at 06:00 and lights off at 18:00).The rats were intraperitoneally injected with LPS (50 μg/kg), AVP (10 μg/kg) or V1a vasopressin receptor antagonist (V1a antagonist, 30 μg/kg) at 10:00 or 11:30.Hyperalgesia was assessed by measuring the latency to withdraw a hindpaw from radiant heat (Hargreaves test).The concentrations of IL-1β and PGE2 in the serum were tested by ELISA.RESULTS: Intraperitoneal administration of LPS induced periods of biphasic fever accompanied by hyperalgesia.AVP reversed LPS-induced fever, and decreased the hyperalgesia and BAT thermogenesis.Peripheral administration of V1a antagonist enhanced the fever produced by LPS, but did not affect the hyperalgesia.AVP significantly attenuated LPS-induced IL-1β and PGE2 production.CONCLUSION: Peripheral administration of AVP reverses LPS-induced fever and decreases hyperalgesia by reduction of BAT thermogenesis and inhibition of IL-1β and PGE2.Endogenous AVP attenuates the fever induced by LPS, but does not affect the nociceptive thresholds.
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Objective To study the subcutaneous injection of physostigmine (PHY) inducing hypothermic response and its relationship with endogenous arginine vasopressin ( AVP). Methods Core temperature and motor activity were monitored by telemetry in female rats maintained at an ambient temperature of 25℃. Tail skin temperature was measured at 30 min intervals with digital thermometer. The central cholinergic antagonist, scopolamine ( lmg/kg ) and AVP V_1 receptor antagonist were administered during the period of PHY (0. 25mg/kg) induced hypothermia. Plasma AVP concentration was measured at 50 min after administration of PHY. Results Subcutaneous injection of PHY led to a rapid reduction in core temperature concomitant with a marked elevation in the heat loss from the tail. The hypothermic response of PHY was blocked by scopolamine and AVP V1 antagonist. Plasma AVP concentration increased markedly at 50 min after PHY. Conclusion The results suggest that endogenous A VP could be involved in PHY -induced hypothermic processes. This may be a novel mechanisms of action for a reversible anticholinesterase drug ( such as PHY ) - induced hypothermia.
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Objective To Study wheather the endogenous arginine vasopressin(AVP)is involved in the effect of oxotremorine(a muscarinic receptor agonist)-induced hypothermic response.Methods Core temperature and motor activity were monitored in undisturbed rats using radiotelemetry.Effect of AVP V1 antagonist on oxotremorine(OXO)-induced changes in body temperature and motor activity were observed in the rats.Results Administration of OXO led to a marked hypothermia.Core temperature recovered to basal levels at 4 hours after OXO administration.AVP V1 antagonist blocked markedly the hypothermia effect of OXO.Conclusion The AVP V1-receptor antagonist block the hypothermic effect of OXO,which suggests that OXO-induced hypothermia is mediated by AVP releasing.
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AIM: This study was designed to examine whether endogenous arginine vasopressin (AVP) is involved in soman-induced hypothermic process. METHODS: Core temperature was measured at 60 min intervals with digital thermometer. Effect of AVP V 1 receptor antagonist (30 ?g/kg, ip) on soman-induced hypothermia was observed in rats, and plasma AVP concentration was measured at 2 h after administration of soman(60 ?g/kg, sc). RESULTS: Administration of soman led to a marked hypothermia. Core temperature recovered to basal levels at 7 h after soman treatment. Plasma AVP concentration increased markedly at 2 h after soman treatment, and administration of AVP V 1 receptor antagonist markedly blocked the hypothermic effect of soman. CONCLUSION: The data indicate that AVP is involved in soman-induced hypothermia in the rat.
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AIM: To assess if endogenous arginine vasopressin is involved in normal thermoregulatory processes. METHODS: Core temperature was monitored in undisturbed rats using radiotelemetry. Effect of AVP V 1 antagonist on normal body temperature were observed in rats under a 12:12 light-dark cycle. RESULTS: Intraperitoneal injection of AVP V 1-receptor antagonist in rats induced a increase in normal body temperature. Under normal light (light on at 6:00 AM-6:00 PM), AVP V 1 antagonist induced a increase in body temperature persisting for about 6 hour, but male rats had higher hyperthermia than female. Under normal dark exposure (light off at 6:00 PM- 6:00 AM), AVP V 1-receptor antagonist caused a increase in body temperature persisting for about 2 hour at the start of the dark phase, but no difference was found between sexes. CONCLUSION: Intraperitoneal injection of AVP V 1-receptor antagonist caused a increase in normal body temperature. The data indicated that endogenous vasopressin could be involved in tonic thermoregulatory process.