Pulsatile GH secretion is under the control of two hypothalamic peptides, growth hormone-releasing hormone (GHRH) and somatostatin (somatotropin release-inhibiting factor/SRIF). Our current understanding comes from a series of classical experiments which demonstrated that SRIF modulates GH trough levels and is important in the inhibition of GH secretion, whereas GHRH regulates pulsatile GH release from the anterior pituitary gland (6).
The timing of a spontaneous GH surge influences the effect of GHRH on GH secretion. Identical doses of GHRH stimulate a greater GH secretory response when administered during a spontaneous GH secretory episode, a time when SRIF is low, as compared to a GH trough when SRIF secretion is increased (7). A variety of neuromodulators (neurotransmitter, pharmacologic, cytokine, and so forth) capable of disrupting this intrinsic rhythm, enhance GH secretion by inhibiting somatostatin release or by stimulating GHRH release. Neurotransmitters involved in GH secretion include adrenergic, dopaminergic, cholinergic, and serotonergic pathways (8,9).
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