The arterial baroreflex (Jordan, 1995) regulates blood pressure (MABP) by changing sympathetic vasomotor tone and heart rate (HR). Acute hypothermia at a core temperature (T_b) of 25 °C caused a greater fall in HR than MABP, and decreased the pulsatility of renal sympathetic nerve activity (RSNA) (Sabharwal et al. 2001). The present study aimed to determine whether these changes were due to the influence of the hypothalamic thermoregulatory centre on central drive or a direct hypothermic effect on the periphery. This was done by generating baroreflex curves for HR and RSNA at T_b = 37 °C, on cooling to T_b = 25 °C and rewarming to 37 °C.

Male Wistar rats, 290-320 g, were anaesthetised with fluothane (2.5 % in O₂) and α-chloralose/urethane (32/450 mg kg^-1 I.V.). MABP and HR were measured via a femoral artery. A renal nerve bundle to the left kidney was placed on recording electrodes to measure integrated RSNA (%). Deep oesophageal T_b was regulated by means of a thermostatted plate. Baroreflex curves were generated using bolus doses of phenylephrine (10 µg) and sodium nitroprusside (10 µg) and the responses in HR and RSNA to a change in MABP were recorded and fitted to logistic function curves (Kent et al. 1972). Responses were compared between normothermic (n = 6) and cold-acclimated (n = 7) rats (Sabharwal et al. 2002). Rats were killed with an overdose of sodium pentabarbitone. Data (means ± S.E.M.) were analysed using ANOVA and significance taken at P < 0.05.

In both groups of animals, the baroreflex-HR curve was completely suppressed at T_b = 25 °C with a reduction of ~30 % (P < 0.01) in maximum response from 440 ± 3 b.p.m., ~95 % (P < 0.01) in response range from 75 ± 10 b.p.m., and ~10 % in midpoint pressure from 123 ± 17 mmHg at T_b = 37 °C. The reduction in maximum gain at T_b = 25 °C was 96 and 60 % in normothermic and cold-acclimated rats from -0.9 ± 0.2 and -1.6 ± 0.7 b.p.m. mmHg^-1, respectively (P < 0.01). The baroreflex-RSNA curve, with maximum response at 70 ± 14 %, response range at 154 ± 18 %, and maximum gain at -2.3 ± 0.7 % mmHg^-1 at T_b = 37 °C, were reduced by 26 and 70 % (P < 0.05), 12 and 40 % (P < 0.05) and 13 % (P < 0.05) and 40 % (P < 0.01) at T_b = 25 °C in normothermic and cold-acclimated rats, respectively. All parameters returned towards precooling levels on rewarming. The suppression of baroreflex control of sympathetic nerve activity may contribute to the modest hypotension observed during hypothermia, whereas the marked bradycardia may be due to cooling of the sinus node and increased vagal tone. The data suggest that baroreflex control of HR during hypothermia is mediated peripherally rather than centrally.