Failure of chronic aldosterone infusion to increase arterial pressure in dogs with angiotensin-induced hypertension.

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Abstract
To generate quantitative data relating to the hypertensive activity of aldosterone, 9 .mu.g/kg per day (4 times normal) aldosterone (4-ALDO) was infused chronically in both adrenalectomized and intact dogs until steady state conditions were achieved. Mean arterial pressure (MAP) was monitored continuously, 24 h/day, and daily steady state values for MAP based on approximately 600 sample points per day were determined by using computerized data analysis. In some studies, angiotensin II (A II) was also infused chronically (5 ng/kg per min) prior to and during 4-ALDO administration to maintain plasma levels of A II constant. 4-ALDO infusion in intact dogs maintained on 75 meq Na/day increased MAP by only 13 mm Hg, compared to a greater than 30 mm Hg rise observed with A II infusion alone, even though plasma aldosterone concentration rose in these experiments only 2/3 as much as when 4-ALDO was infused. When A II was infused chronically, a fall in plasma A II concentration could not compensate for the hypertensive effects of superimposed 4-ALDO infusion; maximal aldosterone-induced hypertension was expected. In both adrenalectomized and intact dogs, the further addition of 4-ALDO failed to increase the degree of A II-induced hypertension and failed to promote Na retention. Chronic A II infusion in intact dogs maintained on 75 and 190 meq Na per day produced a sustained increase in plasma aldosterone concentration (2.7 and 1.6 times control, respectively) as well as kaliuresis and hypokalemia. Infusion of A II in adrenalectomized dogs produced hyperkalemia, not hypokalemia. Apparently, high plasma levels of aldosterone, at least over several weeks, have only weak hypertensive effects in the dog, particularly when aldosteronism is associated with a primary increase in A II.