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

To generate quantitative data relating to the hypertensive activity of aldosterone, 9 /xg/kg per day (4 times normal) aldosterone (4-ALDO) were infused chronically in both adrenalectomized and intact dogs until steady state conditions were achieved. Mean arterial pressure (MAP) was monitored continuously, 24 hours per day, and daily steady state values for MAP based on approximately 600 sample points per day were determined by employing computerized data analysis. In some studies, angiotensin II (A II) was also infused chronically (5 ng/kg per min) prior to and during 4ALDO administration to maintain plasma levels of A II constant. 4-ALDO infusion in intact dogs maintained on 75 mEq sodium per 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 two-thirds 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; therefore, maximal aldosterone-induced hypertension was expected. However, 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 sodium retention. Chronic A II infusion in intact dogs maintained on 75 and 190 mEq sodium 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. The data indicate that high plasma levels of aldosterone, at least over a period of several weeks, have only weak hypertensive effects in the dog, particularly in instances in which the aldosteronism is associated with a primary increase in A II.