Responses of the isolated, perfused human spleen to sympathetic nerve stimulation, catecholamines and polypeptides.

1. The responses of the smooth muscle of the capsule and blood vessels of the isolated, perfused human spleen to sympathetic nerve stimulation, adrenaline, noradrenaline, angiotensin, oxytocin, vasopressin, isoprenaline and acetylcholine have been investigated and compared with those of dog spleen.2. Stimulation of the postganglionic sympathetic nerves to the human spleen at frequencies of 3-10 Hz evoked graded vasoconstriction but very small changes in spleen volume.3. The injection of adrenaline and noradrenaline in doses of 0.25-25 mug to the human spleen produced graded increases in splenic vascular resistance with very small decreases in spleen volume.4. Administration of the alpha-adrenoceptor blocking drug phenoxybenzamine completely abolished or considerably reduced the vascular responses of the human spleen to sympathetic nerve stimulation or the injection of noradrenaline.5. The vascular action of adrenaline was often reversed to elicit a vasodilatation after phenoxybenzamine suggesting the presence of beta-adrenoceptors in the vascular bed. This was confirmed by the administration of isoprenaline which induced a marked reduction in vascular resistance of the human spleen.6. The polypeptides angiotensin and vasopressin induced a marked vasoconstriction in the human spleen without changes in the spleen volume. These effects were uninfluenced by the administration of phenoxybenzamine.7. The polypeptide oxytocin caused a slight vasodilatation in the human spleen, an effect almost exactly mimicked by the preservative chlorobutanol.8. Preliminary experiments suggest that noradrenaline is the transmitter released by the postganglionic nerves to the human spleen.9. These results provide direct evidence that the normal human spleen, unlike that of the dog, does not have a reservoir function. It is suggested that contractions of the enlarged human spleen may occur in various pathological conditions.