The effects of metabolic and respiratory acidosis on renal function in a stable isolated perfused rat kidney preparation were studied. In response to metabolic acidosis, the perfusate pH fell to 7.15 and the perfusate HCO3- fell to 13.6 ± 1 mM. Urine flow increased from 8.2 ± 1 to 33.8 ± 4 μl/min, and U(Na)V increased from 0.608 to 3.3 μeq/min. During a comparable degree of respiratory acidosis, no fall in perfusate HCO3- was seen and an increase in urine flow and U(Na)V did not occur. In response to metabolic acidosis a significant increase in potassium excretion occurred, from 0.22 to 0.5 μeq/min. However, such a response was not seen during respiratory acidosis. A significant positive linear correlation was seen between U(K)V and U(Na)V (r = 0.8, P < 0.001). The isolated kidney also failed to reduce urinary pH below 6 in response to an acid load. The authors conclude that the natriuresis, diuresis, and kaluresis seen with metabolic acidosis can be attributed to decreases in perfusate bicarbonate concentration rather than to changes in pH per se. It is also suggested that the kaluresis observed during metabolic acidosis is a function of increased urine flow and distal sodium delivery resulting from depressed perfusate HCO3 concentration. The failure of the isolated kidney to acidify urine maximally suggests that this preparation may be a model of distal renal tubular acidosis.
