The water intake in hypertensive rats was investigated. Rats made hypertensive by renal ischemia increased their water consumption by 75 per cent over the preoperative level. Polyuria was associated with this polydipsia and the independence of these occurrences from a number of other factors was demonstrated.
It was found that the presence of a normal kidney exerted a compensatory influence which may mask either hypertension or polyuria or both. The appearance or exacerbation of the changes upon removal of the normal kidney, on the one hand, and the elimination or mitigation of the symptoms upon removal of the ischemic kidney on the other support the view that the changes observed cannot have been due to passive elimination of the kidney tissue by ischemia, but to active malfunction of the renal, and especially the tubular, mechanism upon withdrawal of oxygen. The view is put forward that polyuria is a primary sequel of ischemia rather than secondary to the intra- and extrarenal effects of hypertension. A number of concomitant observations are in harmony with this hypothesis.