Abstract
Parathyroid hormone (PTH) has been known to produce phosphaturia in a variety of species (Agus et al., 1971; Amiel et al., 1970; Bell et al., 1972). This response is most strikingly demonstrated in individuals with primary hyperparathyroidism, in whom excess phosphaturia and hypophosphatemia correlate closely with measured elevations in serum PTH levels (Aurbach and Heath, 1974). On the other hand, the role of PTH in the regulation of phosphate (PO4) homeostasis in normal subjects has been more difficult to ascertain. For example, studies from several laboratories have revealed that a variety of agents may influence the urinary excretion of PO4 in the absence of PTH including extracellular fluid volume expansion (Amiel et al., 1970), diuretics (Fulop and Brazeau, 1968), the level of dietary PO4 intake (Steele, 1976), insulin (DeFronzo et al., 1976), mild hyperglycemia (DeFronzo et al., 1976), phlorizin infusion (Nussbaum et al., 1978), and changes in systemic pH (Fulop and Brazeau, 1968; Puschett and Goldberg, 1969).
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
