BIOL 3327 Lecture Notes - Lecture 39: Canrenone, Spironolactone, Ace Inhibitor
Document Summary
Like spironolactone, they are competitive antagonists for the aldosterone receptor, preventing the increase in activity, preventing the loss of na+ and we get more k+ reabsorption (major clinical effect). Oral; gets to its receptor by just floating around in the blood, but is strongly bound to plasma albumin. Canrenone (active metabolite), gets converted in the liver (primarily the responsible therapeutic action) Increase na+ concentration in the tubular fluid. Increased na+ delivered to collecting ducts decreases k+ Prevent na+ from being reabsorbed at the end in the collected duct. Saves our k+ from being taken out of the blood and brought into the collecting duct based on the ratio. Because it blocks the last 2% ofthe sodium, it boosts up the effects of the thiazides/loop diuretic. By itself, they will lose na+ being absorbed back into the blood. Risk increases when agents are given with other drugs/supplements that elevate. K+ directly (k+ supplements) or indirectly (ace inhibitors) or with renal disease.