Abstract
The phosphaturic action of parathyroid hormone (PTH) is mediated via stimulation of adenylate cyclase at the basal pole of the cells of the proximal convoluted tubules, with a resultant increased synthesis of 3′, 5′ adenosine monophosphate (c’AMP).1 Some of the newly formed c’AMP enters the circulation but most passes into the cell. Together with increased entry of calcium, this decreases entry of phosphate into the luminal pole of the cell.2 We have examined the steady-state relationship between serum immunoreactive PTH (iPTH) and renal production of c’AMP (nephrogenous c’AMP or Nc’AMP) in subjects with varying levels of parathyroid function and normal renal function and in patients with chronic renal failure. We have also examined the steady-state relationship between these two independent indices of PTH secretion and the tubular maximum reabsorption of phosphate/unit of GF (TMP/GFR) as an index of phosphaturic action of PTH.
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© 1980 Plenum Press, New York
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Kleerekoper, M., Cruz, C., Bernstein, R.S., Levin, N.W., Foreback, C.C., Parfitt, A.M. (1980). The Phosphaturic Action of PTH in the Steady State in Patients with Normal and Impaired Renal Function. In: Massry, S.G., Ritz, E., Jahn, H. (eds) Phosphate and Minerals in Health and Disease. Advances in Experimental Medicine and Biology, vol 128. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9167-2_19
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DOI: https://doi.org/10.1007/978-1-4615-9167-2_19
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4615-9169-6
Online ISBN: 978-1-4615-9167-2
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