Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

Abstract

The role of parathyroid hormone (PTH) and of Ca⁺⁺ in the regulation of bicarbonate absorption (RHCO₃) and its response to extracellular volume expansion (VE) was studied in HCO₃^--loaded dogs. VE lowered RHCO₃ in both intact (from 24.8 to 22.0 mmol/liter GFR, P < 0.01) and thyroparathyroid-ectomized (TPTX) (from 24.5 to 18.0 mmol/liter GFR, P < 0.001) dogs; glomerular filtration rate (GFR) and filtered HCO₃^- did not change. Both groups showed a significant increase in the fractional excretion of sodium (C_Na × 100/GFR), calcium (C_Ca × 100/GFR), and chloride (C_Cl × 100/GFR) and a decrease in phosphorus reabsorption. Fractional clearance of phosphate (C_P × 100/GFR) rose in both groups but did not achieve significance. Infusion of purified parathyroid extract (PTE) decreased RHCO₃ in intact dogs (from 24.6 to 22.5 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.9 to 22.6 mmol/liter GFR, P < 0.05). No change was noted in GFR, renal blood flow (RBF), filtered HCO₃^-, or fractional excretion of sodium, calcium, or chloride in either group. There was a significant increase in fractional phosphorus clearance and a decrease in phosphorus reabsorption in each group. Infusion of Ca⁺⁺ raised ultrafilterable Ca⁺⁺ from 5.7 to 7.9 mg/100 ml in intact and from 4.9 to 7.2 mg/100 ml in TPTX dogs; RHCO₃ increased in intact (from 22.9 to 26.9 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.6 to 28.6 mmol/liter GFR, P < 0.05). The GFR, RBF, and the fractional excretion of sodium, chloride, and calcium did not change in either group. The reabsorbed phosphate increased in both groups, and fractional phosphorus clearance fell in the intact group but did not change significantly in the TPTX group. Superimposition of PTE on hypercalcemia in TPTX dogs resulted in a decrease in RHCO₃ (from 27.3 to 23.9 mmol/liter GFR, P < 0.001), which was accompanied by an increase in the fractional excretion of phosphate and a decrease in the reabsorbed phosphate. In this group of TPTX dogs hypercalcemia caused a drop in RBF from 135.6 to 105.8 ml/min with no change in GFR. The RBF returned to control value with PTE infusion. It is concluded that: (a) the lowering of RHCO₃ by VE is not dependent solely on stimulation of PTH by the lowered Ca⁺⁺, (b) PTE acts directly on the renal tubules to lower RHCO₃, (c) Ca⁺⁺ enhances RHCO₃ and this effect is exerted in the absence of PTH and calcitonin, (d) neither the effects of Ca⁺⁺ nor of PTH appear to be mediated by altered hemodynamics, although this cannot be excluded in Ca⁺⁺-infused TPTX dogs, (e) Ca⁺⁺ enhanced phosphate reabsorption in the absence of PTH; this may be a specific effect of hypercalcemia on phosphate reabsorption or the nonspecific consequence of the rise in serum phosphorus.