How do calcium channel blockers counteract the sodium retention effect of NSAIDs?

Calcium channel blockers counteract the sodium retention effect of nonsteroidal anti-inflammatory drugs (NSAIDs) primarily by having a direct natriuretic effect. NSAIDs tend to cause sodium retention through their inhibition of prostaglandin synthesis, which reduces renal blood flow and promotes sodium reabsorption in the kidneys, leading to increased blood pressure.

Calcium channel blockers, on the other hand, work by relaxing the smooth muscles of blood vessels, which lowers blood pressure and enhances renal perfusion. This facilitates the excretion of sodium through the kidneys, thus counteracting the sodium-retaining effects of NSAIDs. Their mechanism includes improved renal function and a natriuretic response, which supports the body in balancing sodium levels and helps mitigate the hypertension induced by NSAID use.

In contrast, options that imply mechanisms such as inhibiting potassium reabsorption or directly acting as diuretics do not accurately describe how calcium channel blockers function in this context. While they do support improved renal function and can influence diuretic effects, their primary action against sodium retention from NSAIDs is through their natriuretic effect. Additionally, increasing blood viscosity does not relate to the mechanism of action of calcium channel blockers or their role in counteracting