The best case for a physiological effect of GH in the CNS is inhibition of its own release, as part of an autofeedback circuit (74). Experiments in chronically cannulated rats (using GHs from other species to permit measurement of endogenous rat GH) have repeatedly confirmed that GH inhibits its own secretion (75-78) rapidly blocking spontaneous pulsatility (Fig. 5). Indirect evidence in humans also supports the notion of GH autofeedback (79,80), but it is more difficult to interpret since it is obviously difficult to distinguish exogenous and endogenous GH in humans.
Carlsson et al. used continuous infusions of hGH in conscious rats to compare the effects on spontaneous GH secretion, and found equivalent inhibition in both males and females (46). However, this blockade was readily overcome by GHRH injections in females, but not in males, suggesting that the relative effects on GHRH inhibition and SRIF stimulation might differ in the sexes. These studies did not address the involvement of GH feedback in setting the spontaneous pulse rhythm, but when pulsatile GH was given to conscious male rats, a resetting of the spontaneous pulse generator to the exogenous GH feedback rhythm was evident (81). This could reflect "driving" a regular SRIF rhythm in this experiment. Although this is an artificial situation, it is possible that it indicates an involvement of GH in setting an oscillation in SRIF, and the fall in this sets the timing of subsequent GH pulses. Infusion of hGH blocks the rebound secretion of GH following cessation of SRIF infusion in female rats (78) and it would be interesting to see if a "male" type rhythm of GH release could be established in female rats by trains of hGH pulses as it can by SRIF withdrawal.
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