Acute hypothermia causes a reduction in renal blood flow (RBF), glomerular filtration rate (GFR), natriuresis and diuresis, even though mean arterial blood pressure (MABP) is largely unchanged (Sabharwal et al. 2001). This implies an increase in renal vascular resistance (RVR) occurring primarily at the afferent arteriole, and a possible rise in the neurally mediated vascular tone (Broman et al. 1995). This study aimed to correlate the changes in the pattern of renal sympathetic nerve activity (RSNA) to cardiovascular and renal functions cooling to 25 °C and on rewarming back to 37 °C, and to compare the response in normothermic and cold-acclimated rats.

Male Wistar rats, 290-320 g (n = 14 normothermic, n = 12 cold-acclimated), were anaesthetised with fluothane (2.5 % in O₂ ) and maintained with α-chloralose/urethane (32/450 mg kg^-1) via a femoral vein cannula. MABP and heart rate (HR) were measured via a femoral artery cannula interfaced with a digital recording device. An infusion of 1.5 % inulin in saline (150 mM NaCl at 3 ml h^-1) was used for the estimation of glomerular filtration rate (GFR), while urine flow (UV) and absolute sodium excretion (UNaV) were determined from the outflow of the left ureteral cannula. For RSNA experiments, a renal nerve bundle of the left kidney was isolated, placed on bipolar electrodes and the signal subjected to power spectral analysis. Core (deep oesophageal) temperature (T_b) was regulated by means of a thermostatted plate. At the end of experiments, rats were killed with an overdose of sodium pentabarbitone. Cold-acclimated rats were exposed to progressively lower environmental temperature (20 °C to 4 °C) and photoperiod (12 h to 1 h light day^-1) over 8 weeks. Data (means ± S.E.M.) were analysed using ANOVA and significance taken at P < 0.05.

At T_b = 25 °C, there was a ~50 % reduction in HR (418 ± 9 b.p.m. at 37 °C, P < 0.01) but only a ~15 % fall in MABP (111 ± 2 mmHg at 37 °C, P < 0.05). On cooling GFR decreased by ~50 % (4.6 ± 1 ml kg^-1 min^-1 at 37 °C, P < 0.05) in normothermic and by 5 % (3.8 ± 1 ml kg^-1 min^-1 at 37 °C) in cold-acclimated rats. A cold-induced diuresis (40 ± 5 vs. 21 ± 2 µl kg^-1 min^-1, P < 0.05, in normothermic and 47 ± 10 vs. 38 ± 4 µl kg^-1 min^-1 in cold-acclimated at 37 °C) and natriuresis (5 ± 1 vs. 1 ± 1 µmol kg^-1 min^-1, P < 0.05, in normothermic and 5 ± 1 vs. 3 ± 1 µmol kg^-1 min^-1, P < 0.05, in cold-acclimated at 37 °C) was evident at T_b = 25 °C. There was a loss in pulsatility in the RSNA signal while integrated RSNA increased by 20 % (P < 0.05) in normothermic but decreased by 20 % (P < 0.05) in cold-acclimated rats at T_b = 25 °C. There was a progressive fall in proportion of RSNA power at HR frequency with cooling (20 % in normothermic and 80 % in cold-acclimated rats, P < 0.05). On rewarming all variables, in both groups of rats, returned to basal levels. We conclude that the natriuresis and diuresis in normothermic rats during hypothermia is a consequence of a reduction in nephron reabsorption and possibly due to the altered patterning of RSNA. In cold-acclimated rats it may be due to altered renal haemodynamics and/or hormonal influences induced by chronic cold exposure.

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