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

Abstract

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

Concepts to utilize in describing thermoregulation and neurophysiological evidence for how the system works

“…Various concepts and advances in the research field of temperature regulation set the stage for the current era, which has involved a detailed characterization of the system, and furthered understanding of the involved nervous structures and effector organs (Nakayama 1985;Nagashima et al 2000;Kanosue et al 2001;Morrison et al 2008;Nakamura and Morrison 2008a, b;Tanaka et al 2009). Interactions between thermal homeostasis and other systems have also received careful analysis, such as during fasting and dehydration (Yoda et al 2000;Nagashima et al 2001Nagashima et al , 2003Nagashima et al , 2005Konishi et al 2002Konishi et al , 2003. In addition to internal systems involved in temperature regulation, the external environment has a definite effect on the body temperature.…”

Endogenous angiotensin II and the regulation of oxygen consumption and colonic temperature in rats

“…ICV administration of the AT 1 antagonist candesartan blocked the decrease in core temperature caused by peripheral administration of hypertonic saline (Konishi et al, 2002) and the decrease in core temperature that accompanies pregnancy in rats (Cairns et al, 2005). In one study (Mathai et al, 2001), ICV losartan increased colonic temperature in rats during heat exposure but not in other studies (Horowitz et al, 1999;Kregel et al, 1994).…”

Central Mechanisms for Thermoregulation in a Hot Environment

“…These responses would be important in preserving body fluid and preventing excessive blood distribution to the periphery; however, animals may lose thermal homeostasis. In contrast, it has been reported that the behavioral response was activated during salt loading in rats and pigeons [71][72][73] . The PO/anterior hypothalamus contains abundant warmsensitive neurons 12) , which are involved in various autonomic and behavioral thermoregulatory processes 17,[73][74][75][76][77] .…”