Corticotropin-induced alkalosis in the weanling rat and its relation to the balance of non-metabolizable base.

Studies of whole body balances of non-metabolizable base (NB) and several electrolytes and of the acid-base status of blood and urine during development of corticotropin-induced alkalosis in the weanling rat were carried out in order to identify the primary source of base and factors instrumental in maintenance of the alkalotic state. The data were compared to baseline and running control values and to the results of whole carcass analysers. Primary accumulation of NB was accounted for by ongoing gastrointestinal NB absorption in the weight-losing animal, distributed to extracellular and non-extracellular compartments of the body. An increase in the rate of renal excretion of non-metabolizable acid (NA), from negative values to zero, corresponded to an increased load of endogenous sulphuric acid and a reduced rate of gastrointestinal NB absorption. Accordingly, the renal response did not per se contribute to the induction of extracellular alkalosis. Maintenance of alkalosis occurred in spite of ample chloride in the renal tubular lumen and a moderate increase in relative extracellular volume. In the absence of evidence of overloading (with base) or malfunction of the kidney, corticotropin-induced alkalosis is classifiable as a 'set-point disturbance' of acid-base metabolism in which fluctuations in the (non-renal) load of NA lead to commensurate changes in renal NA excretion at an elevated extracellular pH. Withdrawal of corticotropin injections was followed by prompt restoration of a normal extracellular acid-base status and a return to reference values for renal NA excretion despite a marked fall in the balance of NB. This observation supports a concept of the extracellular compartment as the immediate reference system of the kidney.