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CHANGES IN PLASMA ALDOSTERONE FOLLOWING THE ADMINISTRATION OF VARIOUS COMBINATIONS OF STIMULI

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ABSTRACT The effects on plasma aldosterone levels of combinations of the main factors involved in aldosterone regulation have been studied in normal young male subjects. These factors, namely K, angiotensin II and ACTH were studied using combinations of K+ with angiotensin II, K+ with ACTH, and angiotensin II with ACTH. KC1 infused in amounts (5–10 mEq./h) insufficient to increase plasma aldosterone by itself was found to potentiate the aldosterone response to an infusion of angiotensin II (7 ng/kg/min) in 8 out of 13 subjects. The same amount of KCl was also found to increase the rise in plasma aldosterone following an infusion of ACTH (16 ng/kg/min). When an angiotensin II infusion was superimposed on the last 2 h of a 4-h infusion of ACTH, a striking rise in plasma aldosterone was observed, which exceeded the values obtained by ACTH alone. Conversely, when an ACTH infusion was superimposed on the last 2 h of a 4-h angiotensin II infusion, a further increase of plasma aldosterone was again observed. Our data support the idea that changes in all the known stimuli of aldosterone secretion have to be taken into account when interpreting changes in plasma aldosterone. Thus KCl, infused at rates without effect on aldosterone when given alone, will increase aldosterone during angiotensin II or ACTH infusion. The data also demonstrate that no refractory period is observed when one stimulus is superimposed on a previous one.
Title: CHANGES IN PLASMA ALDOSTERONE FOLLOWING THE ADMINISTRATION OF VARIOUS COMBINATIONS OF STIMULI
Description:
ABSTRACT The effects on plasma aldosterone levels of combinations of the main factors involved in aldosterone regulation have been studied in normal young male subjects.
These factors, namely K, angiotensin II and ACTH were studied using combinations of K+ with angiotensin II, K+ with ACTH, and angiotensin II with ACTH.
KC1 infused in amounts (5–10 mEq.
/h) insufficient to increase plasma aldosterone by itself was found to potentiate the aldosterone response to an infusion of angiotensin II (7 ng/kg/min) in 8 out of 13 subjects.
The same amount of KCl was also found to increase the rise in plasma aldosterone following an infusion of ACTH (16 ng/kg/min).
When an angiotensin II infusion was superimposed on the last 2 h of a 4-h infusion of ACTH, a striking rise in plasma aldosterone was observed, which exceeded the values obtained by ACTH alone.
Conversely, when an ACTH infusion was superimposed on the last 2 h of a 4-h angiotensin II infusion, a further increase of plasma aldosterone was again observed.
Our data support the idea that changes in all the known stimuli of aldosterone secretion have to be taken into account when interpreting changes in plasma aldosterone.
Thus KCl, infused at rates without effect on aldosterone when given alone, will increase aldosterone during angiotensin II or ACTH infusion.
The data also demonstrate that no refractory period is observed when one stimulus is superimposed on a previous one.

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