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SUMMARY Purified human urogastrone was given by intravenous infusion to 12 normal volunteer subjects and measurements made of gastric acid, pepsin and intrinsic factor secretion, and of plasma gastrin concentration. Clinical, haematological, and biochemical screening tests were made throughout the period of study. Urogastrone inhibited acid and intrinsic factor secretion whether stimulated by pentagastrin, histamine, or insulin, but had a much less marked effect on gastric pepsin output. Plasma gastrin levels did not alter significantly. Limited dose-response studies showed that 0.25 ,g urogastrone kg-' hr-1 resulted in inhibition of acid output of 80 % and was not associated with clinical side-effects. No significant alteration in any of the haematological or biochemical measurements was observed in any of the subjects.

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SUMMARY Our earlier observation that pentagastrin is a calcitonin (CT) secretagogue was confirmed and extended to include both synthetic human gastrin I and pure porcine gastrin II. The latter hormone was shown to stimulate the secretion rate of CT from thyroid preparations perfused in situ in anaesthetized pigs at concentrations (0·5 nmol/l) similar to those found after stimulation of gastrin production by a meat extract placed in the stomach (0·2 nmol/1). These concentrations of plasma gastrin are considerably less than those found in man in both pernicious anaemia and the Zollinger—Ellison syndrome, whereas the mean fasting plasma gastrin concentrations in normal human beings and pigs are similar. It is suggested that the comparatively high incidence of parathyroid hyperactivity in association with the Zollinger—Ellison syndrome may be a consequence of an increased CT secretion rate induced by hypergastrinaemia. Furthermore, the existence of a gastrointestinal—thyroid C cell system is proposed as an integral part of postprandial calcium homeostasis.