Dk. Arya et al., COMPARISON OF THE EFFECTS OF HIGH AMBIENT-TEMPERATURE AND CLONIDINE ON AUTONOMIC FUNCTIONS IN MAN, Naunyn-Schmiedeberg's archives of pharmacology, 355(3), 1997, pp. 376-383
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.