To investigate the effect of metabolic acidosis on intestinal calcium (Ca) and phosphorus (P) absorption and vitamin D metabolism, metabolic balance studies and in vitro gut sac uptake of 45Ca and [32P]phosphate were performed in rats maintained on low-Ca and moderately low-P diet and fed NH4Cl for 3 or 9 days and pair-fed controls. Plasma 1,25(OH)2D concentration was measured in the rats fed NH4Cl for 9 days and their controls. Net Ca and P absorption was 87-92% in the acidotic rats and did not differ from control. Moreover, gut sac uptakes of 45Ca and [32P]phosphate were not different from control. Plasma 1,25(OH)2D was higher in the ammonium chloride-fed rats than in controls (213 +/- 44 vs. 110 +/- 12 pg/ml), and serum P was lower in the acidotic animals (4.6 +/- 0.7 vs. 7.6 +/- 0.3 mg/dl). These data indicate that metabolic acidosis does not depress the augmented intestinal absorption of calcium and phosphorus noted during their dietary deprivation nor reduce the plasma level of 1,25(OH)2D.

We examined the effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on intestinal 45Ca and [32P]phosphate uptake in normal and mineral- and vitamin D-replete adult rats. The results indicate that 45Ca uptake by adult rat duodenum was stimulated by "physiological" doses of 1,25(OH)2D3. With increasing dosage of 1,25(OH)2D3, 45Ca uptake also became stimulated first in the colon and then in the jejunum and ileum. The increase in duodenal and jejunal 45Ca uptake was paralleled by an increase in [32P]phosphate uptake, but this parallelism was not always seen in the ileum and was never observed in the colon. The dissociated calcium and phosphate transport response to 1,25(OH)2D3 stimulation in the colon was further confirmed by the measurement of transmural fluxes using a modified Ussing technique. These responses to 1,25(OH)2D3 are similar to those observed in younger vitamin D-deficient rats. However, supraphysiological doses of 1,25(OH)2D3 caused weight loss in normal adult rats, whereas the same metabolite, even when given in large doses, led to weight gain in vitamin D-deficient rats. We propose the normal adult rat as an additional model for evaluating the biological action of 1,25(OH)2D3.