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40 patients with primary hyperparathyroidism, 2 with and 38 without previous surgery had computed tomography (CT) and ultrasonography (US) preoperatively. CT correctly identified enlarged glands in 75%, US in 80%. In 7.5% US was correctly negative. In 12.5% CT has shown only a correct suspicion. Us was false positive in 2.5%, CT in 5%. US was false negative in 10%, CT in 7.5%.

The effects of gastrointestinal hormones on cAMP accumulation and parathyroid hormone (PTH) release were investigated in dispersed bovine parathyroid cells. Secretin (10 (-7) M) caused a 4- to 6-fold increase in cAMP accumulation, while glucagon, vasoactive intestinal peptide, and gastrin caused little if any stimulation. Cholecystokinin caused a 2- to 3-fold increase in cAMP accumulation at 10(-6) M, but this effect may be related to contamination with endogenous secretin since synthetic cholecystokinin octapeptide had no effect. Maximal intracellular cAMP accumulation due to 10(-7) M secretin was reached within 5 min and returned to control over the next 30-60 min, concomitant with a progressive rise in extracellular cyclic nucleotide. cAMP accumulation was half-maximally stimulated by 5 x 10(-9) to 1 x 10(-8) M secretin and was unaffected by alpha- or beta-adrenergic or dopaminergic blockers. Parallel effects were noted on PTH release : 10(-8) M secretin caused a 20-50% increment in PTH release at 15 min which persisted for up to 2 h; PTH release was stimulated half-maximally by approximately 6--8 x 10(-9) m secretin. The specificity of the observed results for secretin and the lack of effect of adrenergic antagonists suggest the presence of a receptor for secretin on dispersed bovine parathyroid cells. These results also suggest the possibility that secretin may modulate parathyroid function in vivo in the cow.