Resting systolic, diastolic, and mean blood pressures (MBP), as well as heart rates, of unanesthetized, unrestrained, cold-acclimated (CA, 4 wk, 6 degrees C) rats were measured by direct arterial cannula and compared with those of controls maintained at 25 degrees C. Exposure to cold increased all these measurements significantly. Mean heart weight of CA rats was also increased significantly above that of controls. The responsiveness of MBP and heart rate to administration of the beta-adrenergic agonist, isoproterenol (3, 5, and 8 micrograms/kg ip), to unanesthetized, unrestrained, CA rats during exposure to air at 6 degrees C was similar to, and possibly less than, that of warm-acclimated (WA) rats measured at 25 degrees C. Acute administration of the alpha-adrenergic agonist, phenylephrine (100 micrograms/kg ip), to CA rats while in air at 6 degrees C induced less of a change in MBP from pretreatment level than was observed in WA rats. However, no differences were observed between groups when changes in heart rate from pretreatment level were compared. A similar statement may be made for a higher dose of phenylephrine (150 micrograms/kg ip), although MBP were elevated to higher levels in both groups with the higher dose. Abrupt exposure of WA rats to cold (6 degrees C) resulted in a sharp increase in heart rate and a more gradual increase in MBP over a period of 1 h. Removal of CA rats from 6 to 25 degrees C resulted in a gradual decrease in heart rate with no significant change in MBP during the ensuing hour.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of the present study was to characterize the sympathetic nerve responses to hyperthermia in chloralose-anesthetized rats. Discharges were recorded from the renal, lumbar, and splanchnic sympathetic nerves. Mean arterial pressure, heart rate, and sympathetic nerve discharge (SND) were recorded continuously during progressive increases in core body temperature (Tc) from 38.0 to 41.0 degrees C. The following observations were made: 1) significant increases in renal, lumbar, and splanchnic SND were observed during hyperthermia; 2) autospectral analysis of renal and lumbar SND revealed that the frequency distribution of SND can be altered during progressive increases in Tc; and 3) increases in splanchnic SND to acute heating were similar in baroreceptor-innervated and -denervated rats. We conclude that 1) hyperthermia is a potent stimulus to the sympathetic nervous system and increases the activity in three sympathetic nerves that innervate different regional arterial beds, 2) acute heating influences the neural circuits involved in generating SND as evidenced by changes in the basic pattern of renal and lumbar SND, and 3) the increase in splanchnic SND during hyperthermia is not opposed by the arterial and cardiopulmonary baroreceptors.

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