Cardiovascular Drugs and Medications Q 41
A clinical instructor asks a nursing student about an aldosterone antagonist. The student is correct by saying that aldosterone antagonists:
A. Create an osmotic gradient.
B. Inhibit the exchange of sodium for potassium.
C. Cause metabolic acidosis.
D. Work poorly in the presence of endogenous aldosterone.
Correct Answer: B. Inhibit the exchange of sodium for potassium.
Aldosterone antagonists compete with endogenous aldosterone and prevent sodium reabsorption in exchange for potassium elimination. Potassium supplements should be discontinued and combination therapy with other drugs that cause hyperkalemia, such as ACE-I and nonsteroidal anti-inflammatory drugs (NSAID), should prompt enhanced electrolyte surveillance. Specifically, serum K+ levels should be reassessed within one week after a change in the prescribed dose of a medication that increases the risk for hyperkalemia when coadministered with an aldosterone receptor antagonist or if there is a change in the patient’s clinical status that influences serum electrolyte levels or fluid balance
Option A: Aldosterone antagonists work on inhibiting the action of aldosterone rather than creating an osmotic gradient. The pathobiological effects of hyperaldosteronism on the cardiovascular system extend beyond increased intravascular fluid retention and volume overload. Hyperaldosteronism causes endothelial dysfunction and impairs vascular reactivity, in part, by decreasing vascular antioxidant capacity, increasing oxidant stress, and limiting bioavailable nitric oxide.
Option C: Aldosterone antagonists do not cause metabolic acidosis. Hyperaldosteronism also activates inflammation; alters fibrinolysis by increasing plasminogen activator inhibitor-1 expression; and promotes tissue fibrosis. Other adverse effects attributed to hyperaldosteronism that may influence cardiovascular function include sympathetic nervous system activation, decreased baroreceptor sensitivity, increased electrolyte excretion (K+, Mg+), and cardiomyocyte apoptosis.
Option D: Aldosterone antagonists must work in the presence of endogenous aldosterone. Aldosterone is synthesized by the adrenal glands to preserve intravascular sodium, potassium, and water homeostasis. Aldosterone binds to mineralocorticoid receptors in the kidney, colon, and sweat glands and induces sodium (and water) reabsorption with concomitant potassium excretion.