Functional Restoration of Pituitary after Pituitary Allotransplantation into Hypophysectomized Rats

Long-term hormone replacement therapy due to panhypopituitarism can lead to serious complications and thus, pituitary transplantation is considered a more desirable. We investigated functional restoration after allotransplatation of the pituitary gland. We transplanted extracted pituitary gland into the omentum of an hypophysectomized rat. Two experiments were performed: (1) to confirm the hypophysectomy was successful and (2) to assess functional restoration after pituitary transplantation. Pituitary hormone level and weight change were consecutively assessed. Electron microscopic (EM) examinations were performed to identify morphological changes at 3 days after transplantation. We confirmed that pituitary gland was properly extracted from 6 rats after sacrifice. The findings showed (1) a weight loss of more than 3% or (2) a weight change of less than 2% along with a decreased growth hormone (GH) level by more than 80% at 2 weeks post-hypophysectomy. A further four rats underwent pituitary transplantation after hypophysectomy and were compared with the previously hypophysectomized rats. All showed rapid weight gain during the two weeks after transplantation. The thyroid-stimulating hormone, prolactin, and GH levels were restored at one week post-transplantation and maintained for 10 weeks. Hypophyseal tissue architecture was maintained at 3 days after transplantation, as indicated by EM. These data suggest that a transplanted pituitary gland can survive in the omentum with concomitant partial restoration of anterior pituitary hormones.

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).