COMPARISON OF THE EFFECTS OF HIGH AMBIENT-TEMPERATURE AND CLONIDINE ON AUTONOMIC FUNCTIONS IN MAN

The effects of two interventions, high ambient temperature, a sympathe tic activator, and clonidine, a centrally acting sympatholytic drug, w ere compared on a number of autonomic functions. Eight healthy male vo lunteers participated in four weekly sessions. Each session was associ ated with one of the following treatments: placebo (physiological sali ne infused intravenously over 10 min) at 20 degrees C; clonidine hydro chloride (1.5 mu g kg(-1) in 10 ml infused intravenously over 10 min) at 20 degrees C; placebo at 40 degrees C; clonidine at 40 degrees C. S ubjects were allocated to treatments and sessions according to a doubl e-blind (for drug condition) balanced design. In each session, the fol lowing indices of autonomic function were recorded: systolic and diast olic blood pressure, heart rate, salivation, body temperature, plasma noradrenaline and adrenaline concentrations, baseline and carbachol-ev oked sweating, physiological finger tremor. Raised ambient temperature (40 degrees C) caused increases in heart rate, body temperature, carb achol-evoked sweating and physiological finger tremor. Clonidine (at 2 0 degrees C) reduced systolic blood pressure, body temperature, saliva tion and plasma noradrenaline concentration, but did not affect any of the other measures. Clonidine (at 40 degrees C) counteracted the incr ease in heart rate, but not the increases in carbachol-evoked sweating and finger tremor, evoked by high ambient temperature. The high ambie nt temperature condition abolished the body-temperature-lowering effec t of clonidine, but did not modify the effects of clonidine on systoli c blood pressure, salivation and plasma noradrenaline concentration. T hese results indicate that while the effects of the heat stressor are consistent with an increase in sympathetic activity, and most of the e ffects of clonidine are consistent with a decrease in sympathetic acti vity, only two functions (body temperature and heart rate) were affect ed in opposite directions by the two interventions. Indeed, physiologi cal antagonism between the two interventions could be demonstrated on body temperature and heart rate only, and there was no evidence for an interaction between the effects of the two variables on any of the ot her indices of autonomic activity. The failure of clonidine to affect two sympathetically mediated functions, carbachol-evoked sweating and physiological finger tremor, under either temperature condition, indic ates that central alpha(2)-adrenoceptors cannot be involved in the reg ulation of these functions.