Jm. Ye et al., ALPHA-ADRENERGIC STIMULATION OF THERMOGENESIS IN A RAT KANGAROO (MARSUPIALIA, BETTONGIA-GAIMARDI), American journal of physiology. Regulatory, integrative and comparative physiology, 40(3), 1996, pp. 586-592
The Tasmanian bettong (Bettongia gaimardi) is a small rat kangaroo wit
hout detectable brown adipose tissue (BAT). In view of our previous fi
ndings of norepinephrine-mediated increase in O-2 consumption (Vo(2))
in the perfused hindlimb of this species, the present study examined t
he effect of alpha-adrenoceptors on the thermogenesis of conscious bet
tongs at rest by infusing adrenergic agents via an indwelling catheter
in the tail vein. The resting Vo(2) was 22.9+/-1.9 mmol . kg(-1). h(-
1) Norepinephrine (10-80 mu g . kg(-1). min(-1)) stimulated V-o2 in a
dose-dependent manner with the maximal increment of 46.7%. Naphazoline
(an alpha(1),alpha(2)-adrenergic agonist) and phenylephrine (an alpha
(1)-adrenergic agonist) also elicited increases in V-o2 with maximal v
alues of 29.6 and 34.8%, respectively In contrast, the alpha(2)-adrene
rgic agonist clonidine had no significant effects. Both alpha- and bet
a-adrenergic blockers were used to antagonize the submaximal increase
in Vo(2) elicited by norepinephrine. At a dose of 10 mu g . kg(-1). mi
n(-1), the alpha-adrenergic blocker phentolamine abolished the effects
of naphazoline and phenylephrine and reduced norepinephrine-induced V
-o2 by 45.5%. The beta-adrenergic blocker propranolol inhibited the no
repinephrine-induced V-o2 by 58.8% at 20 mu g . kg(-1). min(-1). A com
bination of the two antagonists blocked 82.5% of the norepinephrine-in
duced Vo(2). Pretreatment of the animal with indomethacin (1 mg/kg), a
known inhibitor of prostaglandin cyclooxygenase, had no effect on phe
nylephrine-elicited Vo(2). Taken together, these results indicate that
alpha(1)-adrenoceptors are directly involved in norepinephrine-induce
d thermogenesis in non-BAT tissue(s).