Study of the Renal Tubular Interactions of Thyrocalcitonin, Cyclic Adenosine 3′, 5′ -Monophosphate, 25-Hydroxycholecalciferol, and Calcium Ion

Abstract

A B S T R A C T Acute clearance studies were performed in thyroparathyroidectomized animals to determine the actions and interactions of thyrocalcitonin (TCT), cyclic adenosine 3'5'-monophosphate (cAMP), 25-hydroxycholecalciferol (25HCC), and calcium ion on the reabsorption of phosphate, calcium, sodium, and potassium by the kidney. The infusion of 25HCC in a dosage of 60 U/h to moderately saline-expanded animals (2.5% body weight) induced a fall in the excretion of all of the ions under study after 90-120 min similar to that observed in previous experiments from this laboratory. Mean decrements in fractional excretion were: phosphate, 42.0% (P < 0.005); calcium, 25.0% (P < 0.005); sodium, 23.4% (P < 0.001); and potassium, 14.7% (P < 0.005). The superimposition of either porcine or salmon TCT (1-100 MRC U/h for 2 h) resulted in no further alterations in electrolyte excretion. However, the infusion of TCT during steady-state saline expansion, before the administration of 25HCC, obviated the renal transport effects of the vitamin D metabolite. Both in the latter studies, as well as those in whiicl similar doses of TCT were given to hydropenic animnals, the hormone itself failed to induce any consistent alteration in electrolyte excretion. Cyclic AMP (50 mg/h) caused an increase in the excretion of phosphate, sodium, and potassium and no change in calcium excretion. Like TCT, the nucleotide blocked the action of 25HCC on the kidney. Raising the mean level of serum ultrafilterable calcium to 3.02±0.25 mEq/liter from 1.62±0

Behavioral Characterization of d - and l -Amphetamine: Neurochemical Implications

“…This hypothesis would also explain the lack of effect of large doses (up to 25 units per hour) of the metabolite in the absence of PTH. The phosphaturia which occurred with massive doses of 25-HCC may well have reflected alterations induced in bone (23) or in the renal tubular cell (24) which, at this dosage level, may not require further metabolism of the 25-HCC (23).…”

Alterations in vitamin D metabolite, parathyroid hormone and fibroblast growth factor-23 concentrations in sclerostin-deficient mice permit the maintenance of a high bone mass

“…Intra-cellular Ca 2+ binding proteins such as calbindin D 9K and D 28K facilitate the movement of Ca 2+ across the cell [46, 98, 99]. Ca 2+ reabsorption in this segment of the nephron is regulated by a variety of hormones such as PTH [49–51, 97, 100, 101], calcitonin [102, 103], and 1,25(OH) 2 D 3 [52, 53, 55, 56, 94, 104–109]. …”

Renal Tubular Transport of Calcium

“…The hormone may be hypercalciuric (44,164) or hypocalciuric (11,36,167). Quamme (167) reported that physiological doses of calcitonin increased calcium reabsorption in thick ascending limb and distal tubule of the thyroparathyroidectomized rat.…”

“…Vitamin D or its analogues may increase or decrease overall renal calcium reabsorption, depending on the experimental conditions (49,164,165). The usual reported effect of vitamin D or its metabolites is to increase overall renal calcium reabsorption (28, 49, 164, 165) attributable to a distal tubule site of action (196) …”