Abstract

In previous investigations, it was found that rats depleted in parathyroid hormone (TPTX rats) had reduced rates of proximal bicarbonate reabsorption independent on blood calcium levels. In the present work, the role of calcium (Ca2+) in rat proximal tubule bicarbonate reabsorption was studied by in vivo stationary microperfusion. Tubules were perfused at different lumen Ca2+ concentrations in the presence and absence of the calcium ionophore A23187. Bicarbonate reabsorption was not affected by Ca2+ in the range of 0 to 1 mM, but was significantly reduced when 0.5 mM EGTA was added to the 0 Ca2+ perfusates, indicating that only at very low luminal Ca2+ levels, bicarbonate reabsorption ( = H+ secretion) was impaired. These observations indicate that Ca2+ in the tubule lumen is important for the maintenance of normal proximal bicarbonate transport, but the low Ca2+ level necessary to impair this transport mechanism is achieved only in the presence of EGTA, a condition that simulates the absence of parathyroid hormone.

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