CORTICOTROPHIN RELEASING FACTOR (CRF) was the first of the postulated hypothalamic factors controlling the release of hormones from the pituitary gland to be demonstrated biologically1. However, it is extraordinary that after 24 years of research, techniques which have established the identity of the hypothalamic peptides involved in the release of thryotrophin, the gonadotrophins and growth hormone, have been unsuccessful when applied to the search for a factor responsible for adrenocorticotrophin (ACTH) release2,3. Vasopressin invariably releases ACTH from the anterior pituitary, but its partial agonistic properties in vitro4–6, its low potency in vivo7 and the isolation of active CRF fractions with little or no vasopressin activity2,3,8,9 have led to its rejection as a physiological CRF10,11. However, recent immunological and immunocytochemical findings have led to renewed interest in the role of vasopressin in ACTH release. High concentrations of immunoreactive vasopressin have been found in portal blood and a direct vasopressin-neurophysin containing axonal pathway to the hypophyseal portal system, which seems to be under the influence of the adrenal cortex, has been identified12,13. Using a sensitive releasing factor bioassay system, the perfused isolated anterior pituitary cell column14, and various immunological techniques, we have presented evidence to support the idea that vasopressin plays a major part in control of ACTH release6, and we now report the existence of hypothalamic factors with weak, labile CRF activity which potentiate the CRF activity of vasopressin to give it full agonistic properties indistinguishable from crude extracts of rat stalk median eminence (SME). Thus we propose that CRF is vasopressin modulated by other hypothalamic factor(s) released into the hypothalamo-hypophyseal portal system.
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GILLIES, G., LOWRY, P. Corticotrophin releasing factor may be modulated vasopressin. Nature 278, 463–464 (1979). https://doi.org/10.1038/278463a0
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