Figure 5 summarizes the aspects of the interaction of the HPA and magnocellular systems discussed above. Hormones classically considered confined to the magnocellular-neurohypophysial system are found in the parvocellular-long portal system and are known to be paramount in the hypophysiotropic control of ACTH release. It is now clear that hormones from the posterior pituitary can influence the secretion of ACTH via the short portal circulation and, possibly, by recirculation. There is some evidence that circulating AVP may affect adrenal sensitivity to ACTH. Corticosteroids, in addition to inhibiting parvocellular CRH and ACTH release, may inhibit the release of AVP from the neurohypophysis. The converse is also true in that patients with adrenal insufficiency may have an SIAD-like scenario. CRH may be synthesized in, and secreted from, magnocellular OT neurons and may be involved in the control of neurohypophysial function.