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Effect of Long-Term Propranolol Administration on Parathyroid Hormone and Calcium Concentration in Primary Hyperparathyroidism

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Supported in part by Clinical Research Center Grant RR-00044 from Division of Research Resources, National Institutes of Health.

University of Rochester School of Medicine, Rochester, New YorkThomas Jefferson University, Philadelphia, Pennsylvania

University of Rochester School of Medicine, Rochester, New YorkThomas Jefferson University, Philadelphia, Pennsylvania

Ann Intern Med. 1979;91(5):740-741. doi:10.7326/0003-4819-91-5-740
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Beta adrenergic agonists have been shown to stimulate parathyroid hormone (PTH) secretion from isolated parathyroid cells. This action can be blocked with the β-adrenergic antagonist propranolol. This response appears to differ from that due to calcium itself, since β-blockade does not alter tissue response to calcium and high calcium concentration does not suppress the response to β-adrenergic stimuli (1-3). Short-term in-vivo studies in animals (4) and humans (5) have also shown PTH responsiveness to β-adrenergic agonists and elimination of this response by propranolol.

We recently found that propranolol significantly decreased serum levels of PTH, alkaline phosphatase, and the incidence of


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