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

Abstract

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).