Endocrine EflFects on Leukocytopoiesis in the Rat. I. Evidence for Growth Hormone Secretion as the Leukocytopoietic Stimulus Following Acute Cortisol-Induced Lymphopenia
Endocrine hormones were found to mediate the rapid leukocyte repopulation of peripheral blood that occurs within 6 hr of an intraperitoneal injection of cortisol. The thymus and lymph nodes both participate in the proliferative response; the degree of leukopenia and the rate of leukocyte repopulation were both decreased after removal of thymus or lymph nodes. Splenectomy, however, did not alter the rate of leukoycte repopulation. The leukocyte count decreased more rapidly in adrenal—demedullated than in intact or adrenalectomized rats, but the time course of leukocyte repopulation was the same in each group. Hypophysectomy, but not thyroidectomy, prevented leukocyte repopulation within the 6–hr period. 3H—thymidine incorporation into DNA of lymph nodes and thymus, but not spleen, was significantly less in hypophysectomized than intact rats. Evidence for an increased concentration of a hormone that promotes leukocytic proliferation was found in plasma of intact cortisol—treated rats; the uptake of 3H—thymidine was significantly greater in thymus and lymph node tissue incubated with plasma of cortisol—treated rats than with plasma of normal or hypophysectomized rats. Homogenates of anterior pituitary, but not of posterior pituitary or skeletal muscle, prevented cortisol—induced leukopenia in hypophysectomized, adrenalectomized rats primarily by increasing the number of polymorphonuclear leukocytes. Pentobarbital anesthesia prevented leukocyte repopulation in cortisol—treated intact rats. Insulin-induced hypoglycemia promoted leukocytosis in cortisoltreated intact rats but not in hypophysectomized rats. Growth hormone (NIH—GH—S9) opposed cortisol—induced leukopenia in hypophysectomized rats. It is concluded that growth hormone release is a normal leukocytopoietic stimulus following cortisol—induced lymphopenia, and as such represents a normal component of the response to stress. (Endocrinology92: 775, 1973)