Resting catfish excreted a urine with electrolyte concentrations about 1/10; that of blood, with very low concentrations of ammonia and lactic acid, only slightly acid pH, and a small resultant net base excretion.
At 26 °C, the intracellular pH was normally 0.51 units lower than the extracellular pH. Both were depressed following the onset of hypercapnia, but there was compensation for both by 24 h, so that pHi was near control values. Consequently the whole body CO2 pool increased from 1.95 to 4.77m-equiv kg−1 during hypercapnia, with about 1.50 m-equiv by active means, and the other 1.32 by passive (non-bicarbonate) buffering.
The renal response to hypercapnic acidosis was to switch from a small netbase excretion to a net acid excretion, which persisted for up to 10 h, and accounted for about 14% of the total active bicarbonate compensation.
There was no statistically significant renal response to an infused HC1 load, but the whole body base excretion rate declined so as to indicate thatabout 25% of the infused load was excreted in the first 2 h, presumably by the gills.
The catfish kidney appears to participate in acid-base regulation in a significant, but quantitatively minor way, implying that the gills are the principalsite of ion transfer in regulating the whole body SID.