What is the expected effect of aldosterone antagonism by spironolactone?

Aldosterone antagonism by spironolactone leads to increased urine output and potassium retention. This results from spironolactone blocking the action of aldosterone, a hormone that promotes sodium reabsorption and potassium excretion in the kidneys.

When aldosterone is antagonized, the kidneys' ability to reabsorb sodium is reduced. As sodium is not reabsorbed, it remains in the renal tubules, where it draws water along with it due to osmotic principles, leading to increased urine output. Meanwhile, because aldosterone is also responsible for promoting potassium excretion, spironolactone's blockade of aldosterone leads to potassium retention. This is an important aspect of spironolactone's use, particularly in conditions where potassium-sparing effects are desired, such as in certain forms of heart failure or hypertension management.

The other options do not accurately reflect the effects of spironolactone’s mechanism of action on renal function and electrolyte balance. Increased sodium retention contradicts the expected effect, decreased urine output is not associated with diuretics, and increased calcium excretion is not a direct consequence of spironolactone therapy. Understanding these mechanisms helps clarify why increased urine output and potassium retention are the