Rats were treated with furosemide, continuously applied by implanted minipumps, for 6 days. As compensation for the salt lost with the urine the animals drank large amounts of a salt solution ad libitum. This procedure resulted in an enlargement of kidney cortex. Light and electron microscopic studies revealed a proliferation of the distal convoluted tubule (DCT). The proportion of the DCT in the cortical tissue increased from 5.98 +/- 1.3% in controls to 9.54 +/- 1.7% (P less than 0.01) in treated rats. Basolateral cell membrane amplification in DCT cells increased from 17.33 +/- 2.9 to 38.24 +/- 5.8 (P less than 0.0001) in treated rats, while luminal membrane area per unit tubular length did not change. The structural changes after furosemide treatment in the DCT suggest an increase in active transcellular transport capacity of this segment. It is assumed that the chronically altered Na load of the tubular fluid (due to transport inhibition in the thick ascending limb of Henle's loop) delivered to the DCT may specifically stimulate the transport capacity of this segment by augmentation of basolateral cell membrane area. The changes occurring in the segment situated downstream to the one in which the function is impaired by furosemide emphasize the role of tubular fluid composition in the regulation of transport function.