Effect of Testosterone on Growth Hormone Secretion in Female Rats during a Continuous Infusion of Growth Hormone Releasing Factor

The effect of testosterone on growth hormone (GH) secretory pattern during a 6-hour continuous infusion of human GH-releasing factor (GRF) (1–44) NH₂ was observed in unrestrained adult female Wistar rats. Rats had been ovariectomized or sham operated 6 weeks previously. Three weeks after the ovariectomy, the rats received sesame oil or testosterone propionate at a dose of 1 or 2 mg s.c. daily for 21 days. All rats were provided with two indwelling cannulae: one in the right atrium for undisturbed blood collection and the other in the inferior vena cava for vehicle or GRF infusion. Vehicle or GRF was administered by an infusion pump at a dose of 50 ng/kg/min for 6 h. Serial blood specimens were obtained every 20 min. Sham-operated adult female Wistar rats exhibited a high-frequency, low-amplitude pulsatile GH secretion during a 6-hour vehicle infusion. When they received a 6-hour continuous infusion of GRF, the amplitudes of GH pulses and baseline GH values were markedly augmented, but the pulse frequency remained unaltered. The GH secretory pattern during a 6-hour vehicle infusion among ovariectomized rats was similar to that of sham-operated female rats, whereas the magnitude of elevation of GH pulse and baseline level in ovariectomized rats were significantly lower than in sham-operated rats. The ovariectomized female rats that had received 2 mg testosterone for 21 days showed a low-frequency, regularly timed, high-amplitude pulsatile GH secretion, and GH values during the intervening period were low. This GH secretory pattern was indistinguishable from that in adult male rats. During a 6-hour continuous infusion of GRF, baseline GH levels in rats given testosterone were less than one tenth of those in sham-operated female rats, while the amplitudes of the GH pulses were augmented to almost three times that of sham-operated female rats. Thus, the masculine GH secretory pattern was clearly preserved and even exaggerated during the stimulation. The reversal of GH secretory pattern was dependent on the dose of testosterone. GH secretion in the presence of a continuous infusion of GRF is determined largely by phasic release of somatostatin. Therefore, our results suggest that the treatment of adult female rats with testosterone masculinizes the GH secretory pattern by reducing the frequency of intermittent diminution of somatostatin release and augmenting the inhibitory tone mediated by somatostatin during the intervening periods.