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1. Respiratory effects were measured in rats during six hours' anaesthesia with urethane and chloralose. 2. One-hundred min from urethane administration, minute ventilation (VE) was minimal, arterial PO2 was low, arterial PCO2 was high; tidal volume (VT) and respiratory frequency (f) were relatively constant; hypercarbic and hypoxic responses were substantial. 3. Between 100 and 400 min from urethane administration, minute ventilation and frequency increased and became more variable, tidal volume remained relatively constant, arterial PO2 rose to 100 mmHg, PCO2 fell to 37 mmHg; hypercarbic sensitivity increased and hypoxic sensitivity decreased. 4. We conclude that the anaesthetic regime produced initial depression of respiration relative to metabolism but without great loss of respiratory chemosensitivity. The respiratory depression was prolonged by increased dosage with urethane and chloralose. 5. The variations between hypercarbic and hypoxic responses confirm that they operate through separate mechanisms.

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The effect of amosulalol on the accumulation of radioactivity from [3H]-noradrenaline and on the subsequent spontaneous and nerve stimulation-evoked outflow of radioactivity have been investigated in the rat isolated right ventricle. In addition the effect of amosulalol on the contractions of the electrically-driven directly muscle stimulated rat right ventricle to isoprenaline and of the rat isolated aorta to phenylephrine and 5-hydroxytryptamine are reported. Amosulalol at 10(-6)M did not prevent the accumulation of radioactivity from a solution containing [3H]-noradrenaline. The spontaneous outflow of radioactivity, following loading of the ventricle with [3H]-noradrenaline, was increased by amosulalol at 10(-6)M by a cocaine- and idazoxan- insensitive mechanism. The nerve stimulation-evoked outflow of radioactivity was increased by amosulalol (10(-6)M), cocaine (10(-5)M) and idazoxan (10(-7)M). The ability of amosulalol to increase nerve-evoked outflow was maintained in the presence of cocaine but prevented by pretreatment with idazoxan. This suggests that amusulalol is an alpha 2-adrenoreceptor antagonist. The contractile response of the electrically-driven directly muscle stimulated right ventricle to isoprenaline were inhibited by amosulalol at 10(-7) and 10(-6)M with apparent pA2 values of 7.5 and 8.1, respectively. It is suggested that amosulalol at 10(-6)M may have an action additional to beta 1-adrenoreceptor antagonism on the right ventricle. The contractile responses of the rat aorta to phenylephrine were inhibited by amosulalol at 10(-7) and 10(-6)M with a pA2 of 8.6 which was independent of concentration. Amosulalol also reduced the magnitude of the maximal responses of the aorta to 5-hydroxytryptamine.