1In unanaesthetized pigeons, kept at room temperature (20-23 C) the effects on cloacal temperature were examined of catecholamines, phenoxybenzamine and propranolol, injected into the cerebral ventricles. 2 Noradrenaline, adrenaline, dopamine and isoprenaline caused a fall in cloacal temperature. 3 Phenoxybenzamine produced a long-lasting small rise in cloacal temperature. This rise is attributed to removal of the hypothermic effect of noradrenaline released continuously from adrenergic neurones ending in the anterior hypothalamus. Propranolol produced a slight fall in cloacal temperature. 4 The hypothermic effects of noradrenaline, adrenaline and dopamine were prevented by phenoxybenzamine but not by propranolol. They are therefore attributed to activation of ct-adrenoceptors.
5The hypothermic effect of isoprenaline was not prevented by either phenoxybenzamine or propranolol. The effect can therefore not be attributed to activation of either a or ,B-adrenoceptors. Propranolol actually accentuated the isoprenaline-induced hypothermia.
1In unanaesthetized pigeons the effect on cloacal temperature was studied of acetylcholine (ACh), carbachol, atropine and (+)-tubocurarine injected into a cannulated lateral cerebral ventricle. The experiments were carried out at an ambient temperature of 19-25 C. 2 ACh or carbachol injected intraventricularly produced hyperthermia, and in larger doses hyperthermia followed by hypothermia. These were central effects because they were not obtained when these drugs were injected in the same doses intravenously. 3 Atropine injected intraventricularly produced hypothermia which was greater and longer lasting than the hypothermia produced with the same dose of atropine injected intravenously. After the intraventricular injection of atropine the hyperthermic effects of ACh and of carbachol were abolished. 4 (+)-Tubocurarine injected intraventricularly produced a long-lasting hyperthermia in doses which had no effect on temperature when injected intravenously. After the intraventricular injection of tubocurarine the hypothermic effects of ACh and of carbachol were abolished. 5 It is concluded that the effects of ACh and carbachol imitate the effects of ACh released from cholinergic neurones in the central pathway involved in temperature regulation. The hypothermic effect of atropine is attributed to unmasking the activity of continuously released ACh acting on nicotinic receptors, and the hyperthermic effect of tubocurarine to unmasking the activity of continuously released ACh acting on muscarinic receptors.
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