On the Mechanism of the Calorigenic Action
of Catecholamines
O. STRUBELT
With 2 Figures
Abstract
The increase in metabolic rate after injection of adrenaline, noradrenaline and
isoprenaline was the same in anesthetized as in awake rats. Partial or total paralysation of skeletal musculature had no influence on the calorigenic action of the
catecholamines. The contribution of increased cardiac work and augmented body
temperature to sympathomimetic hypermetabolism is minimal. Hence, calorigenic
action of catecholamines is a real increase of basal metabolism. This hypermetabolism is a consequence of the metabolic cycles induced by sympathomimetic
glycogenolysis and lipolysis and is probably mediated by the formation of cyclic
3',5'-AMP.
In spite of many investigations, the cause of catecholamine-induced
calorigenesis is still a matter for discussion [1, 3]. Most investigators have
failed to demonstrate calorigenic action of catecholamines in isolated
tissues [2]. In our experiments, adrenaline did not increase oxygen consumption of rat liver slices. Hence, catecholamines probably do not influence
cellular respiration directly. Many authors, therefore, have postulated that
catecholamine-induced hypermetabolism is not a real increment of basal
metabolic rate but the consequence of increased organ activities [1, 2]. This
hypothesis, however, is neither proved nor refuted.
First we found that increments ot motility do not contribute to catecholamine-induced hypermetabolism. 0.3 mg/kg of adrenaline, noradrenaline or isoprenaline were injected into awake rats and in rats anesthetized
with urethane (1.2 g/kg i.m.). Ambient temperature was 28°C. Oxygen
consumption was recorded continuously during 120 min with NOYON'S
diaferometer. The integrated increase of oxygen consumption over basal
values was the same in awake and anesthetized rats.
To exclude increased involuntary activity of skeletal musculature as a
source of sympathetic hypermetabolism, we performed experiments in
awake rats with the spinal cord destroyed from the first dorsal vertebra
downwards. Although 70 to 80 % of the musculature was paralysed,
of Catecholamines
O. STRUBELT
With 2 Figures
Abstract
The increase in metabolic rate after injection of adrenaline, noradrenaline and
isoprenaline was the same in anesthetized as in awake rats. Partial or total paralysation of skeletal musculature had no influence on the calorigenic action of the
catecholamines. The contribution of increased cardiac work and augmented body
temperature to sympathomimetic hypermetabolism is minimal. Hence, calorigenic
action of catecholamines is a real increase of basal metabolism. This hypermetabolism is a consequence of the metabolic cycles induced by sympathomimetic
glycogenolysis and lipolysis and is probably mediated by the formation of cyclic
3',5'-AMP.
In spite of many investigations, the cause of catecholamine-induced
calorigenesis is still a matter for discussion [1, 3]. Most investigators have
failed to demonstrate calorigenic action of catecholamines in isolated
tissues [2]. In our experiments, adrenaline did not increase oxygen consumption of rat liver slices. Hence, catecholamines probably do not influence
cellular respiration directly. Many authors, therefore, have postulated that
catecholamine-induced hypermetabolism is not a real increment of basal
metabolic rate but the consequence of increased organ activities [1, 2]. This
hypothesis, however, is neither proved nor refuted.
First we found that increments ot motility do not contribute to catecholamine-induced hypermetabolism. 0.3 mg/kg of adrenaline, noradrenaline or isoprenaline were injected into awake rats and in rats anesthetized
with urethane (1.2 g/kg i.m.). Ambient temperature was 28°C. Oxygen
consumption was recorded continuously during 120 min with NOYON'S
diaferometer. The integrated increase of oxygen consumption over basal
values was the same in awake and anesthetized rats.
To exclude increased involuntary activity of skeletal musculature as a
source of sympathetic hypermetabolism, we performed experiments in
awake rats with the spinal cord destroyed from the first dorsal vertebra
downwards. Although 70 to 80 % of the musculature was paralysed,