The effects of the inhibition of the renal carbonic anhydrase on the blood acid-base status in hypercapnic rats.

Arterial blood acid-base status was measured in unanesthetized rats treated with benzolamide (a selective renal carbonic anhydrase inhibitor). These measurements were carried out in rats exposed to different levels of CO2 in air (0-10% CO2) for periods of up to 6 hr. In untreated rats the whole body buffer value showed a continuous increase and after 6 hr of exposure to hypercapnia its value was twice that measured initially. On the other hand, the whole body buffer value of benzolamide treated rats did not change during the 6 hr of exposure to hypercapnia. The whole body buffer value of normal rats, measured after 6 hr of hypercapnia is similar to that reported for chronic (3-5 days) hypercapnia in the normal dog. The whole body buffer value in benzolamide treated rats was similar to that reported for the normal dog and man, during acute CO2 exposures. It is suggested that mechanisms involving the renal carbonic anhydrase are responsible for the significant, rapid changes in the whole body buffer value that take place during the initial phase of acute exposure to CO2 in the rat. This may represent a mechanism of adaptation to burrow hypercapnic conditions.