Fig. 10.10 
The sequence of events that occur in secondary hyperaldosteronism. 
In secondary hyperaldosteronism, circulating renin levels are elevated as a consequence of renal artery stenosis, renal hypoperfusion, or volume depletion. High renin levels, in turn, lead to increased angiotensin II levels and hyperaldosteronism, with concomitant sodium retention and potassium wastage.