Fig. 10.6 
The mechanism of pathophysiological changes that occur in primary hyperaldosteronism. 
The autonomous production and release of aldosterone from the tumour leads to excessive sodium retention and potassium wasting; these occur largely due to the effects of aldosterone on the distal tubule of the kidney. Renin release from the kidney is therefore inhibited and this leads to a fall in circulating levels of angiotensin 11.