Final answer:
Deactivating WNK without compensation would result in decreased sodium reabsorption, as WNK kinases are critical in regulating sodium and potassium balance in the kidney's nephrons.
Step-by-step explanation:
If we made a drug that deactivates WNK with no compensation, the effect would likely be (B) Decreased sodium reabsorption. WNK kinases are a family of protein kinases that are involved in the regulation of electrolyte homeostasis, including sodium (Na+) and potassium (K+) balance. Based on understanding related to aldosterone function and its role in the excretion of potassium and the reabsorption of sodium in the distal tubule, a significant interaction with sodium reabsorption processes is implicated.
The inhibition of WNK kinases would interrupt the usual signaling pathways that promote the reabsorption of sodium in the kidney's nephrons. This is expected to lead to a reduction in sodium reabsorption, causing more sodium to be excreted in urine. Such diminishment in reabsorption comes with additional effects, given the fact that potassium and sodium concentrations often move in opposite directions. Therefore, with decreased sodium reabsorption, less potassium would be secreted, which contradicts option (D). Hence, (A) increased sodium reabsorption is not supported by the inhibition of WNK kinase function.