Growth hormone (GH) secretion has traditionally been considered to be under dual hypothalamic control, being stimulated by a GH-releasing factor (GRF) and suppressed by somatostatin (SRIF), an inhibitory releasing factor (Müller, 1987). These hypothalamic peptides are released into hypophysial circulation in response to stimuli in the internal and external environment, and act at receptors on somatotroph cells to regulate GH synthesis and release. Hypophysial portal plasma, however, also transports other hypophysiotrophic factors to the pituitary gland, and somatotrophs are undoubtedly exposed to other putative GRFs.
Thyrotrophin-releasing hormone (TRH; pGlu-His-Pro-NH2) was the first hypophysiotrophic peptide to be isolated and synthesized chemically and was called TRH because it was found to stimulate thyrotrophin (TSH) release from the pituitary gland (Nelson, 1982). However, since its discovery, TRH has been found to be synthesized in numerous locations throughout the 'diffuse neuroendocrine system', and in addition to its neuroendocrine role in the regulation of