Table 2. Physiologically individualized therapy for resistant hypertension.

Physiologic driver	Primary aldosteronism	Liddle’s variants	Renal renovascular
Renin	Low	Low	High
Aldosterone	High	Low	High
Primary therapy	Aldosterone antagonists (spironolactone, eplerenone) or amiloride where not available	Amiloride is the specific therapy	Angiotensin receptor antagonists, renin inhibitors a
	Rarely surgical		Rarely surgical

After rare causes such as pheochromocytoma, coarctation of the aorta, and licorice consumption are eliminated, most causes of hypertension, and their appropriate therapy, can be identified by measuring plasma renin activity and aldosterone, in a stimulated condition [100], and interpreting them correctly in light of the medications being taken at the time of the measurement [101,102].

^aAngiotensin-converting enzyme inhibitors are less effective at blocking secondary hyperaldosteronism, because of escape pathways for formation of angiotensin II; a major part of their mechanism of action is blocking the breakdown of bradykinin, with resultant increases in nitric oxide. In a way, they can be thought of as similar to long-acting nitrates.