Renin‐dependence of drinking induced by partial aortic obstruction in the dog

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Abstract
Inflation of a balloon implanted in the abdominal aorta above the level of the renal arteries was used to produce partial obstruction to aortic blood flow in trained, conscious mongrel dogs. Following inflation, heart rate and arterial blood pressure downstream from the point of inflation fell, while arterial blood pressure upstream from the point of inflation rose. Central venous pressure was unaltered. In 16 of 18 experiments, balloon inflation led to drinking. Inflations maintained for 3 days led to a sustained increase in daily H2O intakes, but intakes of 0.9% NaCl were unaltered when both H2O and 0.9% NaCl were available to drink. There was a significant inverse correlation between the amount drunk in the first 60 min following balloon inflation and the ratio of the change in the arterial pressure upstream of the obstruction to the change in pressure downstream of the obstruction. In experiments where the inflation was maintained for 90 min, there was no further drinking between the 60th and 90th min. In experiments where the inflation was released after 60 min, there was another bout of drinking between the 60th and 90th min. Plasma renin activity and plasma renin concentration both rose following balloon inflation. Drinking following balloon inflation was abolished by infusion of the competitive angiotensin II antagonist saralasin. Inflation of an aortic balloon to a size that produced drinking in other experiments also led to a reduction in urinary water and electrolyte loss in fluid pre-loaded dogs. Water intake in response to partial aortic obstruction above the level of the kidneys apparently is caused by renin released from the kidneys. The dipsogenic effectiveness of the endogenous renin released is reduced as a result of the simultaneous increase in arterial pressure above the obstruction.

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