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Prenylamine, given orally to 4 healthy male volunteers in a dose of 180 mg/day, for 2 weeks: 1. (a) significantly enhanced the increase in respiratory minute volume in response to exercise; 2. (b) did not significantly influence the resting excretion of dopamine, noradrenaline, adrenaline, homovanillic and vanillylmandelic acid; 3. (c) significantly decreased the usual increase in the excretion of noradrenaline which occured during exercise.

The metabolism of nitroglycerin (trinitrin) was studied in dogs and rabbits. After intravenous injection of nitroglycerin in either species, plasma levels immediately declined and then gradually increased; maximum plasma levels occurred between 10 and 20 min after injection. This peculiar course of the plasma levels was due to redistribution of the drug in different organs. The blood pressure responses to nitroglycerin did not parallel the plasma levels. Pretreatment of rabbits with SKF 525 A, an enzyme inhibitor, or with phenobarbital, an enzyme inducer, markedly influenced the plasma levels but did not affect the vascular effects of nitroglycerin. After oral administration of nitroglycerin, blood pressure was normal despite high plasma levels. The vascular effects of nitroglycerin did not seem to be determined by its metabolism or plasma levels.

Nitroglycerin (trinitrin) was studied in the intact anesthetised dog, in the perfused femoral artery or lateral saphenous vein of the dog and on isolated vessels (strips) of rabbit and dog. The behaviour of a vascular bed after systematic administration of nitroglycerin was dependent on reflex adjustments of sympathetic tone. The vasodilator effects of nitroglycerin on perfused vessels or vascular strips were dependent on the time of its administration; administration during an existing contraction was much more effective than administration before contraction. That is, a contraction was more easily abolished than prevented. This behaviour of nitroglycerin contrasts with that of acetylcholine or papaverine.

Experiments on the isolated perfused dog spleen in which the effect of intra-arterially injected catecholamines and splenic nerve stimulation were studied on vascular resistance, venous outflow and organ weight showed that (a) noradrenaline injection and splenic nerve stimulation provoked an increase in vascular resistance, whereas adrenaline injection was followed successively by a quick increase in perfusion pressure and a pronounced decrease of perfusion pressure, apparently due to a stimulation of vascular β-receptors, and then by a secondary increase in perfusion pressure, (b) the reduction of splenic weight was much less pronounced after noradrenaline injection than after adrenaline injection and splenic nerve stimulation, presumably due to a higher uptake of exogenous noradrenaline by the adrenergic nerve endings in the arterial wall, (c) direct evidence for the presence of vascular β-receptors was obtained by the injection of isoproterenol in isolated spleens maintained at a nearly physiological tone and by splenic nerve stimulation after ɑ-receptor blockade, and (d) the neurotransmitter released on splenic nerve stimulation was identified by paper chromatography as being predominantly noradrenaline together with small amounts of dopamine.