Role of calcium in the decline of phosphate reabsorption during phosphate loading in acutely thyroparathyroidectomized rats.

Abstract

In acutely thyroparathyroidectomized (TPTX) rats infusion of inorganic phosphate leads-after saturation of the reabsorptive system-to a continuous decline of the reabsorptive capacity. The present study is designed to define parameters which are responsible for this phenomenon. Animals are infused a phosphate solution (100 mmol/l, pH 7.4, 0.2 ml/min·kg BW) and a phosphate concentration in plasma of about 5.5 mmol/l is maintained for up to 7 h. While glomerular filtration rate as well as plasma sodium concentration remain virtually constant, plasma potassium concentration initially decreases within the first 4 h of the experiment, but increases again after that period. Phosphate reabsorption declines by some 30%, plasma calcium concentration falls from 1.87±0.03 to 1.11±0.05 mmol/l. The animals develope a mixed respiratory and metabolic alkalosis with a plasma pH of 7.54±0.01, a carbon dioxide tension of 4.66±0.13 kPa (35±1 mm Hg) and a plasma bicarbonate concentration of 28.2±1.3 mmol/l. Phosphaturia leads to osmotic diuresis, to an increase of urine pH and titrable acid. When the elevated plasma pH is normalized phosphate reabsorption continues to decline. When the elevated plasma bicarbonate is lowered no further significant change of phosphate reabsorption is found. When, however, the decreased plasma calcium is restored by infusion of calcium chloride a significant increase of phosphate reabsorption up to control values is demonstrated (P<0.01). From these data we conclude that hypocalcaemia in phosphate loaded TPTX rats is the crucial parameter leading to the decline of renal phosphate reabsorption.