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The intravenous administration of the antiadrenaline drug phenoxybenzamine (Dibenzyline) markedly raised the arterial adrenaline and noradrenaline concentration in dogs lightly anaesthetized with thiopentone. Graded haemorrhage led to a further rise in the amounts of amine. In adrenalectomized dogs, phenoxybenzamine moderately increased the plasma noradrenaline concentration. During haemorrhagic hypotension, previous treatment of adrenalectomized animals with phenoxybenzamine led to a significantly greater rise in plasma noradrenaline compared with that of adrenalectomized animals subjected to haemorrhage without treatment with phenoxybenzamine. Thus, phenoxybenzamine (1) raised plasma amine concentration largely due to adrenal medullary stimulation, and (2) led to increased plasma noradrenaline concentrations during sympathetic stimulation in adrenalectomized animals. The previous administration of phenoxybenzamine reduced the amount of blood which could be withdrawn before final circulatory collapse in both normal and adrenalectomized dogs.
In dogs anaesthetized with pentobarbitone sodium phenoxybenzamine greatly increased the urinary excretion of adrenaline and noradrenaline. This was associated with a transient increase in the volume of urine excreted and a fall in blood pressure. Hexamethonium prevented the effects on the urinary amines and on the blood pressure. Methacholine hypotension induced an increased adrenaline excretion, but no change in noradrenaline. The excretion of adrenaline released following ganglionic stimulation by acetylcholine did not appear to be affected by phenoxybenzamine, but that of noradrenaline was increased. During infusions of adrenaline or noradrenaline, phenoxybenzamine increased the excretion of both adrenaline and noradrenaline.
The responses of strips of rabbit aorta to almost maximal doses of nicotine were less readily antagonized by five antisympathomimetic agents than were comparable responses to noradrenaline. The effect was most marked with dibenamine, ergotamine, and tolazoline: approximately twice the dose of noradrenaline was required to match the test dose of nicotine after treatment with the antagonists. Dose/response curves for nicotine before and after phentolamine 10(-7) indicate that the phenomenon may be reversed with low doses of nicotine and that the release of noradrenaline by nicotine within the tissues is probably a graded response. The pattern of nicotine/phentolamine antagonism in this preparation is consistent with the view that nicotine acts indirectly by releasing a noradrenaline-like substance, and the difficulty found in antagonizing responses to nicotine with antisympathomimetic agents is probably similar to that responsible for failure of atropine to block some parasympathomimetic responses to nicotine.