Abstract
There is a wealth of evidence that the renal actions of parathyroid hormone (PTH) result, at least in part, from receptor- mediated stimulation of adenylate cyclase and a consequent increase in renal cell cyclic AMP. Thus, infusions of cyclic AMP (or its dibutyryl derivative) have been shown to reproduce the physiological effects of PTH on the kidney including inhibition of PO4 reabsorption (1–4), stimulation of distal calcium reabsorption (1, 4) and increased production of 1,25(OH)2D3 (5). Numerous studies have demonstrated PTH-stimulation of adenylate cyclase in renal tissue in vitro, and under certain circumstances nephrogenous cyclic AMP excretion can be used as a valid index of parathyroid function (6).
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