Nine patients with hypomagnesaemia have been studied. Six had magnesium deficiency secondary to malabsorption or diarrhoea and three had excessive urinary losses of magnesium. Hypocalcaemia was also present in eight. Parathyroid hormone (PTH) was measured using amino-terminal and carboxy-terminal specific immunoradiometric assays and also, in one patient, using a cytochemical bioassay. Amino-terminal PTH (N-PTH) varied directly with the concentration of magnesium; carboxy-terminal PTH (C-PTH) was raised in all patients. When magnesium was injected, both N-PTH and C-PTH rose regardless of the initial concentration, indicating that hypomagnesaemia was limiting PTH secretion. The clearance of endogenous PTH was measured in one patient, after injection of magnesium. Seven minutes after reaching its peak, C-PTH had fallen to 69% and N-PTH fell to 22% of its maximum values; the initial half life of N-PTH was less than 2 min. In the same study biologically active PTH (bio-PTH) disappeared rapidly with a half-time of disappearance of 1.2 min. Responsiveness to PTH was measured by the rise in plasma cyclic 3'5'-adenosine monophosphate (cAMP) following PTH injection. The rise in plasma cAMP was inversely related to the concentrations of magnesium and PTH at the time. It is suggested that the concentration of PTH rather than the degree of hypomagnesaemia is the most important factor determining the responsiveness of target tissues to PTH in magnesium deficiency.