The renin-angiotensin-aldosterone complex.
Both the thiazide and loop diuretics have long been known to induce both potassium and magnesium wastage with resultant negative balances of these important intracellular cations. The negative potassium and magnesium balances resulting from diuretic therapy are due primarily to stimulation of the renin-angiotensin-aldosterone complex or secondary hyperaldosteronism. A long experience with an attempt to modify or reduce diuretic-induced potassium depletion by dietary sodium restriction and by the use of antikaluretics has been recorded.
D000450:Aldosterone / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D004347:Drug Interactions; D004656:Enalapril / Q000494:pharmacology; D006801:Humans; D006852:Hydrochlorothiazide / Q000494:pharmacology; D008274:Magnesium / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012083:Renin / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D006852:Hydrochlorothiazide; D000450:Aldosterone; D004656:Enalapril; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D008274:Magnesium; D011188:Potassium