Abstract
Alkalosis, either of metabolic or respiratory origin, alters urinary phosphate excretion in man (1,2), dogs (3–5) and rats (6–10). Thus alkalinization of the urine with infusions of sodium bicarbonate decreases renal tubular phosphate reabsorption. A number of indirect factors have been used to explain the resultant phosphaturia following bicarbonate infusion, including volume expansion, enhanced filtered load, hypocalcemia, and endogenous release of parathyroid hormone (PTH). Alternatively, a direct action of HCO3 − on tubular phosphate could explain the resultant phosphaturia. This could arise from intraluminal alkalinization with an increase in the HPO4 =/H2PO4 − ratio. Bank et al (6) have shown by in vivo microperfusion studies that H2PO4 − is transported more readily by the rat proximal tubule than HPO4 =. These findings however are at variance with findings of Ullrich and colleagues (7,10) suggesting that it is the divalent form which is preferentially reabsorbed. Furthermore, Ullrich et al (10) have demonstrated that intracellular alkalosis in addition to luminal acidosis inhibits transtubular phosphate transport. The interaction of HCO3 − with phosphate has been most extensively examined in the rat (6–10).
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© 1980 Plenum Press, New York
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Wong, N.L.M., Quamme, G.A., Dirks, J.H. (1980). The Effect of Bicarbonate on Anion Reabsorption Along the Dog Nephron. 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_18
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DOI: https://doi.org/10.1007/978-1-4615-9167-2_18
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