Salt loading decreases body core temperature (Tcore) at neutral ambient temperature (26°C) and increases heat-escape/cold-seeking behaviour in desalivated rats. In this study, we tested the hypothesis that brain angiotensin II (AII) and arginine vasopressin (AVP) are associated with these responses. Surgically desalivated rats (n = 28) were administered an injection (s.c., 10 ml kg-1) of either normal saline (154 mM, NS) or hypertonic saline (2500 mM, HS) following an intracerebroventricular injection (10 μl kg-1) of an AII AT1-receptor antagonist (candesartan, 5 μg μl-1), an AVP V1-receptor antagonist ((β-mercapto-β, β-cyclopenta-methylene propionyl1, O-Me-Tyr2, Arg8)-vasopressin, 0.5 μg μl-1), or normal saline (154 mm). Each rat was placed in a behaviour box, first at 26°C for 1 h to allow the measurement of baseline Tcore and movement. The ambient temperature was then elevated to 40°C for the next 2 h, during which time the rat was able to trigger a 0°C air reward for 30 s by moving into a specific area of the box (operant behaviour). The s.c. HS significantly decreased baseline Tcore, at 26°C (36.5 ± 0.1°C) and increased counts of operant behaviour at 40°C (57 ± 3) compared with results obtained following s.c. NS injection (37.4 ± 0.1°C and 42 ± 1, respectively). These responses to s.c. HS were inhibited by the intracerebroventricular injection of AT1 (37.3 ± 0.1°C and 43 ± 2, respectively; P < 0.05) and V1 antagonists (37.2 ± 0.2°C and 42 ± 2, respectively; P < 0.05), although administration of both antagonists with s.c. NS had no effect. These results suggest that brain AII and AVP are involved in the decrease in Tcore observed at neutral ambient temperature and the increase in heat-escape/cold-seeking behaviour in response to osmotic stimulation, via the central AT1 and V1 receptors, respectively.
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