The adaptive response of tubular Pi transport to Pi deprivation is detectable in the whole kidney 24 h after switching rats from a high (HPD) to a low (LPD) Pi diet. A more rapid adaptive response of the Na-dependent Pi transport system located in the luminal membrane of the proximal tubule and its relation with changes in phosphatemia an parathyroid [PTH] status are discussed. Rats were fed HPD and trained to eat their daily ration within 1 h. After 2 wk of equilibration half of the animals received a single LPD ration. The animals were either sacrificed for renal cortical brush border membrane vesicle (BBMV) isolated or used for determining plasma Pi concentration, urinary excretion of Pi and cAMP 1, 2 and 4 h after the end of food consumption. At 2 and 4 h, the Na-dependent Pi transport in BBMV was stimulated by 70 and 140%, respectively, in intact rats exposed for the 1st time to LPD. This response was preceded by a significant fall in plasma Pi concentration (HPD: 2.46 .+-. 0.03, LPD: 2.04 .+-. 0.05 mM), in the urinary excretion of Pi (HPD: 899.0 .+-. 68.1; LPD: 6.5 .+-. 3.3 .mu.mol/ml GFR [glomerular filtration rate]) and cAMP (HPD: 76.9 .+-. 7.4, LPD: 48.2 .+-. 1.4 pmol/ml GF [glomerular filtrate]). This suggested a rapid inhibition of PTH after 1 single LPD feeding. In thyroparathyroidectomized (TPTX) rats the Na-dependent Pi transport system was also stimulated 4 h after LPD, but to a slightly less extent than in intact rats. The Na-dependent Pi transport located in the luminal membrane of the proximal tubule reacts within hours to dietary Pi restriction. This specific tubular response coupled with the hypophosphatemia should account for the rapid decrease in urinary Pi excretion. Although the adaptive response at the BBMV level is also expressed in TPTX rats, inhibition of the PTH-cAMP system could contribute to the rapid adaptation observed in intact animals.