Role of pituitary in K+ homeostasis: impaired renal responses to altered K+ intake in hypophysectomized rats.

The kidneys maintain extracellular K⁺ homeostasis by altering K⁺ excretion to match K⁺ intake. Because this can occur without changes in plasma K⁺ concentrations ([K⁺]), how the kidneys sense K⁺ intake is unclear. We tested the hypothesis that the pituitary plays a critical role in signaling K⁺ intake to the kidneys. If this hypothesis is true, hypophysectomy would impair kidney responses to altered K⁺ intake. Hypophysectomized (Hypox) and sham-operated control rats (n = 8 each) were compared for their abilities to adjust K⁺ excretion during a transition from normal to reduced (to one-third of normal) K⁺ intake, followed by a reversal to normal K⁺ intake. Food was provided only at night, and renal K⁺ excretion was determined both for absorptive (night or feeding) and postabsorptive (day or nonfeeding) periods. In normal rats, both absorptive and postabsorptive renal K⁺ excretion were changed in parallel to the changes in K⁺ intake, indicating a rapid adaptation of normal kidneys to altered K⁺ intake. In Hypox rats, whereas absorptive renal K⁺ excretion was changed in response to changes in K⁺ intake, postabsorptive K⁺ excretion was not responsive (P < 0.001), indicating impaired renal responses to altered K⁺ intake. In addition, Hypox rats, compared with control rats, showed K⁺ intolerance (increases in plasma [K⁺]) upon feeding (i.e., K⁺ intake) at night or following an intravenous K⁺ infusion (P < 0.01), indicating an impairment of acute renal responses to K⁺ intake. These data support that the pituitary plays a key role in the signaling of K⁺ intake to the kidneys (and kidney responses to altered K⁺ intake).