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Hi, in Katzung's it says this of the effect of acetazolamide:
"The major renal effect is bicarbonate diuresis (ie, sodium bicarbonate is excreted); body bicarbonate is depleted, and metabolic acidosis results. As increased sodium is presented to the cortical collecting tubule, some of the excess sodium is reabsorbed and potassium is secreted, resulting in significant potassium wasting (Table 15–1). As a result of bicarbonate depletion, sodium bicarbonate excretion slows—even with continued diuretic administration—and the diuresis is self-limiting within 2–3 days. "
I'd like to know if bicarbonate or sodium is the main substance that is responsible for the osmotic diuresis. If sodium, by combining with bicarbonate in the tubular fluid, is indeed the responsible agent, why would the diuresis be self-limiting due to bicarbonate depletion when there would be no bicarbonate binding to sodium to form sodium carbonate in the tubular fluid?
Thank you!
"The major renal effect is bicarbonate diuresis (ie, sodium bicarbonate is excreted); body bicarbonate is depleted, and metabolic acidosis results. As increased sodium is presented to the cortical collecting tubule, some of the excess sodium is reabsorbed and potassium is secreted, resulting in significant potassium wasting (Table 15–1). As a result of bicarbonate depletion, sodium bicarbonate excretion slows—even with continued diuretic administration—and the diuresis is self-limiting within 2–3 days. "
I'd like to know if bicarbonate or sodium is the main substance that is responsible for the osmotic diuresis. If sodium, by combining with bicarbonate in the tubular fluid, is indeed the responsible agent, why would the diuresis be self-limiting due to bicarbonate depletion when there would be no bicarbonate binding to sodium to form sodium carbonate in the tubular fluid?
Thank you!