Renin-angiotensin-aldosterone pathway

Development and progression of heart failure involves activation of neurohormonal pathways, including the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). 

Indomethacin appears to be the NSAID most frequently associated with the development of hyperkalemia, including patients without apparent risk factors [58]. In addition to the known effects of NSAIDs on potassium delivery to the distal tubule and their inhibition of the renin-angiotensin and aldosterone pathways, indomethacin may have a direct effect to limit cellular uptake of potassium [59]. 

Aldosterone is produced exclusively by the zona glomerulosa and is primarily controlled by the renin-angiotensin system (p. 1.5). The metabolic pathway for the synthesis of aldosterone has many of the same enzymes involved in cortisol biosynthesis. The glomerular z.one lacks the 17-hydroxylase enzyme and has the additional 18-hydroxylase and 18-hydroxysteroid dehydrogenase enzymes necessary for aldosterone synthesis. 

Aldosterone is the primary mineralocorticoid. It retains sodium (and subsequently water) in the blood. It is stimulated in the renin-angiotensin pathway. 

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