Sodium and calcium are normally reabsorbed in parallel in the renal tubule. Both parathyroid hormone (PTH) and thiazide diuretics may influence this relationship. This study was designed to show whether the dissociation of Na from Ca transport produced by thiazides is dependent upon the presence of PTH. Hydropenic thyroparathyroidectomized (TPTX) dogs were given chlorothiazide alone and together with PTH. Chlorothiazide alone significantly increased fractional excretion of sodium (0.5 +/- 0.3-5.6 +/- 0.3%) and calcium (0.74 +/- 0.18-1.4 +/- 0.24%). However, the Ca/Na excretion ratio fell markedly from 1.57 to 0.24%. Micropuncture revealed this dissociation to occur at the distal tubule. Proximal reabsorption of water, sodium, and calcium were inhibited to an equal extent. However, distal fractional sodium reabsorption fell 10% whereas calcium reabsorption remained unchanged following chlorothiazide administration in TPTX animals. When phosphaturic doses of PTH were administered with chlorothiazide, no significant changes were observed in calcium or sodium reabsorption. It is concluded that PTH plays no role in the dissociation of sodium from calcium reabsorption resulting from acute chlorothiazide administration.

Micropuncture studies were performed in 26 dogs with a unilateral remnant kidney to examine its response to modest extracellular volume expansion and furosemide administration in the presence (Stage II) and absence (Stage III) of an intact contralateral kidney. During hydropenia in 15 Stage II dogs, proximal and distal transport of sodium and potassium was comparable to that of normal dogs (Stage I). Following 3% volume expansion, fractional proximal reabsorption was reduced similarly in Stages I and II. Although a slightly greater reduction in fractional loop reabsorption of sodium in Stage II after volume expansion was not significant, it was significantly greater with furosemide administration. In 11 Stage III dogs, proximal fractional reabsorption was depressed during hydropenia, and the loop sodium response to both volume expansion and furosemide administration was exaggerated. In contrast, greater increase in distal potassium secretion was demonstrated mainly in Stage III but not in Stage II remnant kidneys both before and after the diuretic maneuvers. The observations of exaggerated sodium response to furosemide by the remnant kidney in both Stages II and III but greater potassium response only in Stage III suggest that independent factors are responsible for these adaptations when functioning renal mass is reduced.