Brown, E.M., Metab. Dis. Branch, Nat. Inst. Arthrit. Metab. Digest. Dis., NIH, Bethesda, Md. 20014, United States
Hurwitz, S., Metab. Dis. Branch, Nat. Inst. Arthrit. Metab. Digest. Dis., NIH, Bethesda, Md. 20014, United States
Aurbach, G.D., Metab. Dis. Branch, Nat. Inst. Arthrit. Metab. Digest. Dis., NIH, Bethesda, Md. 20014, United States

The effects of β adrenergic agonists and antagonist on cyclic AMP (cAMP) accumulation and parathyroid hormone (PTH) release from isolated bovine parathyroid cells have been determined. Beta adrenergic agonists markedly stimulate cAMP production and PTH release with an order of potency (-)isoproterenol > (-)epinephrine >>(-)norepinephrine, suggesting a β2 type adrenergically mediated process. Both effects are blocked by the β blocker propranolol with the strict stereospecificity expected for a β adrenergic response. Low calcium concentrations also stimulate cAMP accumulation, but the cyclic nucleotide response under these conditions is only 3% of that obtained with isoproterenol, raising the possibility that factors other than cAMP may control low calcium mediated PTH release. The release of PTH by low calcium is also not blocked by propranolol, confirming the independence of the response to low ambient calcium from the β adrenergic receptor. These studies substantiate further the utility of the isolated parathyroid cell preparation for studying secretagogue mediated alterations in cyclic nucleotides and hormone secretion. Isolated cells also make feasible the direct identification of β adrenergic receptors in parathyroid cell membranes and whole cells.