CORTICOTROPE AND MELANOTROPE POMC-DERIVED PEPTIDES IN RELATION TO INTERRENAL FUNCTION DURING STRESS IN RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)

Plasma levels of ACTH, alpha-MSH, and N-ac-beta-END, and in vitro interrenal ACTH sensitivity were investigated in rainbow trout (Oncorhynchus mykiss) stressed by confinement and in unstressed fish treated with exogenous cortisol. Within 3 hr after the onset of confinement, plasma cortisol and ACTH levels were significantly elevated above control values, while plasma alpha-MSH, but not N-ac-beta-END, levels were significantly decreased compared with those of unstressed fish. At 3 hr, sensitivity of the interrenal tissue to ACTH stimulation in vitro was reduced in stressed fish compared to that of unstressed controls. This hyposensitivity cannot be due to the intervention of alpha-MSH or N-ac-beta-END, because after 48 hr of confinement levels of both POMC-derived peptides were significantly lower than in controls, whereas interrenal tissue of stressed fish still responded significantly less to an ACTH challenge than tissue from control fish. Plasma cortisol and ACTH levels in confined fish at this time point were similar to those at 3 hr. Within 96 hr of the onset of confinement, plasma ACTH levels in stressed fish had returned to baseline levels. Plasma cortisol levels in stressed fish at 96 hr had also declined significantly, but were still higher than those in controls. The circulating cortisol level cannot be the regulatory factor responsible for the ACTH hyposensitivity observed after 3 and 48 hr of stress, because treatment of unstressed fish with exogenous cortisol (which resulted in elevated plasma cortisol and lower plasma ACTH and alpha-MSH levels compared to those of controls) did not induce a reduction in interrenal sensitivity to ACTH. It is suggested, instead, that these data support the contention that not only the initiation of the interrenal stress response, but also the habituation of the response, are regulated at the level of the hypothalamus via circulating ACTH levels. (C) 1995 Academic Press, Inc.