Final answer:
Primary hyperaldosteronism doesn't cause significant peripheral edema due to compensatory mechanisms like natriuretic peptides and the limited water retention in relation to sodium reabsorption, which prevents substantial increases in interstitial fluid.
Step-by-step explanation:
The question addresses why primary hyperaldosteronism does not result in significant peripheral edema, even though it involves increased aldosterone levels, which typically promote water and sodium retention. In primary hyperaldosteronism, while aldosterone is excessively produced, leading to increased sodium and water reabsorption, the body has compensatory mechanisms, such as the increased excretion of sodium and water promoted by natriuretic peptides and pressure natriuresis. Additionally, increased sodium reabsorption does not necessarily translate to increased water reabsorption to the same extent due to the counter-regulatory effects of other hormones and the body's homeostatic mechanisms, such as the release of atrial natriuretic hormone (ANH), which reduces sodium reabsorption. Consequently, there's not a substantial increase in interstitial fluid volume that would lead to peripheral edema.