Systemic salt loading decreases body temperature and increases heat-escape/cold-seeking behaviour via the central AT1 and V1 receptors in rats

Salt loading decreases body core temperature (T-core) at neutral ambient temperature (26degreesC) 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 mul kg(-1)) of an AII AT(1)-receptor antagonist (candesartan, 5 mug mul(-1)), an AVP V-1-receptor antagonist ((beta-mercapto-beta, beta-cyclopenta-methylene propionyl(1), O-Me-Tyr(2), Arg(8))- vasopressin, 0.5 mug mul(-1)), or normal saline (154 mm). Each rat was placed in a behaviour box, first at 26degreesC for 1 h to allow the measurement of baseline T-core and movement. The ambient temperature was then elevated to 40 degreesC for the next 2 h, during which time the rat was able to trigger a 0 degreesC 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 degreesC (36.5 +/- 0.1 degreesC) and increased counts of operant behaviour at 40degreesC (57 +/- 3) compared with results obtained following s.c. NS injection (37.4 +/- 0.1degreesC and 42 +/- 1, respectively). These responses to s.c. HS were inhibited by the intracerebroventricular injection of AT(1) (37.3 +/- 0.1 degreesC and 43 +/- 2, respectively; P < 0.05) and V-1 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 AT(1) and V-1 receptors, respectively.