Systemic salt loading decreases body temperature and increases heat-escape/cold-seeking behaviour via the central AT₂ and V₁ receptors in rats

Salt loading decreases body core temperature (T_core) 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 T_core 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 T_core, 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 T_core 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.