Abstract

The role of vasopressin as a possible mediator of the inhibition of evaporative water loss (EWL) in dehydrated, heat-stressed cats has been examined by intravenous (i.v.) and intracerebroventricular (i.c.v.) injections of arginine vasopressin (AVP). In normally hydrated cats exposed to an ambient temperature (Ta) of 38°C, neither EWL nor body temperature (Tb), measured in the hypothalamus, was significantly altered by i.v. AVP infusion. Measurements of plasma osmolality (pOsm), pAVP and cerebrospinal fluid AVP (csfAVP) were made normally hydrated cats at Tas of 25 and 38°C and after dehydration for 1–4 days at these temperatures. The relationship between pOsm and pAVP can be described equally well by either a linear model or a log-linear model ( r = 0.81 for both models). The pOsm-csfAVP relationship is best described by alog-linear model ( r = 0.80). A possible role for intracranially released AVP in ody temperature regulation and control of EWL was examined by injecting various doses of AVP into the lateral ventricles of normally hydrated cats. No effect of AVP injection on Tb was observed at either a Ta of 23°C or 38°C. EWL was also unaffected by i.c.v. AVP administration at a Ta of 38°C. To confirm futher that intracranial AVP is not responsible for elevation of Tb and reduction of EWL during dehydration and heat-stress, specific antiserum to AVP was injected into the ventricle of dehydrated animals at a Ta of 38°C. No sinificant effect on either Tb or EWL was measured subsequent to antiserum infusion. These negative findings indicate that AVP does not suppress EWL by either a peripheral or a central action and is therefore not responsible for lowered EWL and elevated Tb seen in dehydrated heat-stressed cats.

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