1. The effects of the orally active converting enzyme inhibitor, captopril (SQ 14225), on blood pressures and intakes and urine outputs of water and electrolytes were studied in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) and in Long Evans rats (parent strain).
2. Captopril given in the drinking water (30 mg day−1 kg−1) caused an increase in fluid intake and urine output in both strains of rat; the difference between intake and measured output did not change.
3. Captopril caused a significant natriuresis wnen given to animals in the non-steady state but did not significantly affect the urinary electrolyte excretion of animals in a steady state; in the latter group, however, captopril caused a significant reduction in food intake. Hence, under both conditions, captopril caused a reduction in sodium balance.
4. Systolic blood pressures were reduced by captopril (given in the drinking water) in Long Evans rats and in Brattleboro rats; there was no accompanying change in heart rate.
5. Bolus administration of captopril (30 mg day−1 kg−1) either intragastrically or subcutaneously did not change the fluid intakes or outputs in either strain of rat.
6. In a separate experiment, rats were given the choice to drink water or a captopril solution. The results showed that the increased fluid intake in response to captopril was not due to a liking for the taste of the solution.
7. The dipsogenic response to captopril may have been due to the fall in blood pressure which occurred, leading to renin release and a peripheral build-up of angiotensin I, which was converted into angiotensin II in the central nervous system. The possibility that the same dose given as a bolus may have inhibited central, as well as peripheral, converting enzyme activity is discussed.