PubMed1989
In the male rat, GH secretion is characterized by high amplitude pulses that appear at regular intervals of 3-4 h, with low basal levels between such pulses. In the female, the pulses are irregular and more frequent, with lower amplitudes, while basal secretion is higher. The present study was designed to exclude the indirect effects of sex steroids on the pituitary, enabling investigation of the direct effects of sex steroids on the pituitary. Rats were gonadectomized at 22 days of age, and 12 days later their anterior pituitaries were trypsinized for cell dispersion. Testosterone (T) or 17 beta-estradiol (E2), 5 nM, was added to the medium for 6 days, and subsequently, GRF or somatostatin was added for 4 h. In a perifusion system, the male-derived cell response to GRF was augmented after pretreatment with T, but not with E2. The female-derived cell response to GRF was augmented by E2, but not by T. T increased the sensitivity of the cells to GRF from 3.0-0.03 nM and increased the maximal potency of GH secretion 3-fold. E2 had no significant effect on the sensitivity, but lowered the potency. Somatostatin (1 nM) inhibited GH secretion by 44% in T-treated cells. In E2-treated cells, somatostatin was ineffective. GRF increased the total amount of GH (medium plus cells) in both T- and E2-treated cells, but not in control pituitary cells. It is suggested that T has direct effects on the male somatotroph. By increasing the pituitary cell responses to GRF and somatostatin, T contributes to the high amplitude peak/low baseline pattern of the male. By decreasing the pituitary cell responses to GRF and somatostatin, E2 contributes to the low amplitude peak/high baseline pattern of the female.