Effects of growth hormone (GH)-releasing hormone and somatostatin on GH secretion from individual human and monkey fetal anterior pituitary cells: modulation by thyroid hormones and glucocorticoids.

A reverse hemolytic plaque assay was used to measure the GH responses of fetal pituitary cells to GHRH, SRIH, T3 and glucocorticoids. Cells from eight human abortuses (18-22 weeks' gestation) showed accelerated plaque formation after treatment with 10(-7) mol/L GHRH-(1-44) [25.6 +/- 0.6% (+/- SE) of cells formed plaques (PFC); mean area, 14.5 +/- 2.7 X 10(4) micron2; all at 1 h], while 10(-7) mol/L SRIH-(1-28) slowed plaque formation (8.6 +/- 0.6% PFC; mean area, 4.2 +/- 0.8 X 10(4) micron2) vs. control (13.7 +/- 0.7% PFC; mean area, 5.3 +/- 0.8 X 10(4) micron2; all at 1 h). The proportion of PFC was equal in GHRH-treated and control groups by 4 h, suggesting that GHRH affects the amount of GH secreted per somatotroph rather than the number of cells that are preferentially responsive to GHRH. Qualitatively similar data were obtained using pituitary cells from four near-term rhesus fetuses. When cells were cultured in defined medium for 3 days, supplementation with T3 reduced basal GH secretion and attenuated the responses to GHRH. Culture with dexamethasone increased basal GH secretion and restored the responsiveness to GHRH. Dexamethasone also caused a shift in plaque area frequency distributions to patterns similar to those in serum-supplemented medium. We conclude that fetal somatotrophs are responsive to SRIH, GHRH, T3, and dexamethasone. Furthermore, glucocorticoids can maintain a subpopulation of fetal somatotrophs in the GHRH-responsive state.