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The present study was performed to investigate the effect of food intake on thermoregulatory vasodilatation in seven healthy male volunteers. The changes in oesophageal (Toes) and mean skin temperatures, finger and forearm blood flows (BF), oxygen consumption (VO2) and heart rate (fc) with and without food intake were measured before and during a 40-min exercise at an intensity of 35% maximal O2 consumption at an ambient temperature of 25 degrees C. Exercise commenced 60 min after food intake. Ingestion of food equivalent to 50.2 kJ.kg body mass-1 elevated mean body temperature, BF, VO2 and fc in 60 min. Four subjects responded to exercise with a marked increase in finger BF and with no sweating (non-sweating group), while the other three responded with perspiration over almost the whole skin area and with little change in finger BF. Further analyses were made mainly in the non-sweating group. The postprandial increases in Toes, BF, VO2 and fc were persistent during exercise. The rate of increase in finger BF with the increase in Toes and mean body temperature was significantly greater with food intake than without. However, there was no difference in the response of forearm BF to exercise between the two conditions. These results suggested that food intake enhanced finger BF response to the increase in deep body temperature during exercise. It was also concluded that there was a regional difference in cutaneous vasomotor response to thermal load in the postprandial subjects.

The mechanisms of the hypothermic effect of angiotensin II (AII) injected into the lateral ventricle were investigated in unanesthetized rats at an ambient temperature of 18 degrees C. Mean blood pressure (BP), heart rate (HR), metabolic rate (M), colonic temperature (Tcol), and temperatures of the interscapular brown adipose tissue (TBAT), and the tail skin (Tsk) were continuously monitored. AII at a dose of 5 micrograms produced a sharp and marked elevation in BP accompanied by bradycardia, and a decrease of M and Tco1 in the sinoaortic baroreceptor intact rats. The difference between TBAT and Tcol decreased significantly, which suggests a suppression of nonshivering thermogenesis of the BAT. Tsk was not changed by the AII injection. After sinoaortic denervation, however, the decrease in Tcol and M with AII injection was significantly reduced despite a marked elevation in BP. In addition, intravenous arginine-vasopressin antagonist pretreatment suppressed the elevation in BP and the decrease in HR, Tcol, and M after AII injection. From these results, it is concluded that the hypothermia which occurred after AII injection into the lateral ventricle can be largely attributed to the baroreflexive suppression of M, and to some extent to the direct effect on the thermoregulatory center in rats.

Intravenous injection of vasopressin (lysin-8-vasopressin, LVP) in unanesthetized rats at an ambient temperature of 18 degrees C caused a decrease in heat production (M) followed by a fall in colonic temperature (Tco1). These changes were preceded by an elevation of aortic blood pressure (BP) and bradycardia, and were related to the dosage of LVP administered. Temperature of the interscapular brown adipose tissue (BAT) significantly fell after LVP injections. Therefore, it can be said that the decrease in metabolism by the peripheral LVP is at least partly due to suppression of BAT thermogenesis. After bilateral sino-aortic deafferentation, however, the changes in these variables were greatly but not completely reduced except for the elevation of BP. LVP of 0.25 micrograms, more than sufficient to cause a significant elevation of BP when administered peripherally, had no effect on M and Tco1 when injected into the anterior hypothalamus. From these results, we conclude that the hypothermic effect of vasopressin administered peripherally is largely attributed to the baroreflexive suppression of nonshivering thermogenesis, and is not due to the action on the temperature regulatory centers. The slight but insignificant suppression of metabolism in the sinoaortic denervated rats following injection of LVP may be caused by a decreased blood flow to the thermogenic tissues.

Atrial temperature (Tat), heat production (M), mean arterial blood pressure (BP), and feeding (FA) and locomotor (LA) activities were measured over a 24-h period in spontaneously hypertensive rats (SHR) and their normotensive controls (Wistar Kyoto rats; WKY) at an ambient temperature of 24 degrees C. Clear day-night changes in all variables were observed in both groups except for BP and LA in SHR. During the day (0600-1800 h), SHR moved more frequently and seemed to eat more food than WKY. However, the total amount of food consumed for the 2 consecutive days was the same in both SHR and WKY. Compared with WKY, average M and BP during the day and at night and FA and LA during the day were significantly higher in SHR. The responses of Tat for a 24-h period, M during the day and for a 24-h period, and BP during the day to FA were significantly enhanced in SHR. There were no such significant differences of responses in Tat, M, and BP to LA between SHR and WKY. The results suggest that SHR is hyper-responsive in metabolism and blood pressure to feeding activity, particularly in the daytime, but not to locomotion.

The effects of chronic administration of naloxone (120-150 micrograms X kg-1 X h-1) on the wheel running activity (WR) and on food and water intakes were studied in male Wistar rats subjected to a 2-h restricted feeding (1200-1400 h) schedule at 24 +/- 1 degrees C and LD 12:12 (L: 0600-1800 h) cycle. The restricted feeding significantly increased WR before and after the feeding time. Food and water intakes per day were reduced and body weight gradually decreased for the 2-week food restriction period. Food and water intakes appeared to be suppressed by naloxone, particularly shortly after the administration. The chronically administered naloxone slightly increased the 24-h WR. In the naloxone-treated rats, the fraction of WR before the feeding time (anticipatory activity) was significantly increased compared with saline-treated rats. The fraction of WR after the feeding time (succeeding activity) did not change. These results suggest that the endogenous opioid system may play a role in suppressing the excess increase in the anticipatory locomotor activity in the food restricted rats.

The effects of intracerebroventricular (icv) vasoactive intestinal polypeptide (VIP), secretin, glucagon, and cholecystokinin-octapeptide (CCK-8) on the thermoregulatory and cardiovascular systems were studied in conscious rats. The icv injection of VIP at a dose of 10 micrograms produced hyperthermia with an increase in the positive difference between the interscapular brown adipose tissue (BAT) and colonic temperatures (TBAT-Tco), but had little effect on nonevaporative heat loss. Mean arterial blood pressure and heart rate increased following the icv VIP. The results were consistent at ambient temperatures (Ta) of 18, 23, and 28 degrees C. The icv injection of secretin at doses of 1 and 10 micrograms at Ta of 23 degrees C produced hypothermia with a decrease in (TBAT-Tco) and elevated blood pressure without any change in heart rate. The 10 micrograms of icv glucagon had no effect on the thermoregulatory and cardiovascular systems. The large dose of icv CCK-8 (10 micrograms) induced persistent hyperthermia. Nonsulfated-form CCK-8 and CCK-tetrapeptide, however, were ineffective on all variables measured. These results indicate that the central VIP activates BAT thermogenesis and induces hyperthermia, but has a minimum effect on nonevaporative heat loss. Although VIP, secretin, and glucagon have similarities in terms of chemical structure, their effects on body temperature, BAT thermogenesis, and the cardiovascular system are quite different.

Angiotensin II (AII, 5 micrograms) injected into the cerebral ventricles produced hypothermia in conscious rats at ambient temperatures (Ta) of 18, 23, and 28 degrees C. At Ta of 18 and 23 degrees C, AII-induced hypothermia was attributed to both enhancement of heat loss and suppression of metabolic rate. At Ta of 28 degrees C, AII-induced hypothermia seemed to be mainly attributed to increased heat loss.

The effects of intraventricular neurotensin (NT) at doses of 0.1, 1.0, and 10.0 micrograms on blood pressure (BP), heart rate (HR), heat production (M), heat loss (H), and colonic temperature (T co1) were investigated in conscious rats in a direct calorimeter at 18 and 28 degrees C. At 18 degrees C, a 10.0 micrograms of NT significantly increased BP for several minutes after injection with prolonged bradycardia. The larger two doses (1.0 and 10.0 micrograms) significantly reduced M and T co1. In sinoaortic denervated rats, a 1.0 microgram of NT elevated BP and decreased HR. The decrease in HR was significantly smaller than that in nerve intact rats, which indicates the occurrence of baroreflex with intraventricular NT. The changes in M and T co1 in the denervated rats were, however, not statistically different from the intact rats. The baroreflexive suppression of metabolism seems to play a minimum role in the NT-induced hypothermia. H slightly increased for several minutes after central NT (1.0 and 10.0 micrograms) and significantly decreased thereafter. Thermal conductance significantly increased for a longer period of time after NT injection. At 28 degrees C, 1.0 microgram of NT increased H and M. It is concluded that central NT produced hypothermia by reducing M and enhancing H in the cool environment, but not at 28 degrees C.

Changes in blood pressure, heart rate, and heat balance during febrile response to E. coli endotoxin were studied in unanesthetized guinea pigs at an ambient temperature of 24 degrees C. The heat balance was measured with direct and indirect calorimetry. An intravenous injection of endotoxin (5 micrograms X kg-1) produced characteristic biphasic changes in the intra-aortic temperature (Tar), heat production (M), and heat loss (H). The response of arterial blood pressure (BP) to the endotoxin was monophasic and that of heart rate appeared triphasic. Phenylephrine (PHE: 20 micrograms X kg-1 X min-1) infused intravenously in the two rising phases of fever increased BP to the same extent, but the amount of the reflexive bradycardia seemed to be less during the first rise of Tar. The increased metabolism (shivering and nonshivering thermogenesis) during fever development was suppressed by PHE infusion at the two rising phases. The results conclude that, in guinea pigs, the baroreflexive suppression of metabolism is persistent during fever development, but the reflex sensitivity may be different at different phases of fever.

The effects of intraventricular bombesin (BS) at doses of 0.1, 1.0, and 10.0 micrograms on thermoregulatory and cardiovascular functions were studied in conscious rats with a direct calorimeter at ambient temperatures (Ta) of 18, 23, and 28 degrees C. At two lower TaS, the central BS produced a profound decrease in colonic temperature (Tcol) with a reduction of the temperature difference between the interscapular brown adipose tissue (BAT) and the colon (TBAT-Tcol). Increases in nonevaporative and evaporative heat losses and mean arterial blood pressure (BP) were consistent following the central BS at any dose tested at any Ta. In the sinoaortic deafferentated rats, a 0.1 microgram of BS produced hypothermia with a significant decrease in (TBAT-Tcol) and heat production (M). Changes in Tcol, (TBAT-Tcol), and M in the denervated rats, however, were not different from those in the sham-operated rats. These results suggest that the central BS suppresses BAT thermogenesis and facilitates heat loss mechanisms. The baroreflex-mediated metabolic reduction is not the case in the BS-induced hypothermia in rats.