Cortisol inhibits the ACTH-releasing activity of urotensin I, CRF and sauvagine observed with superfused goldfish pituitary cells.
The structurally homologous peptides urotensin I, ovine CRF and sauvagine stimulate the release of immunoreactive ACTH from a superfused dispersed goldfish anterior pituitary cell column. The addition of cortisol to the superfusion buffer resulted, following a latent period, in a decrease in basal release of ACTH from the pituitary cell column and a diminution in the ACTH-releasing activities of urotensin I, CRF and sauvagine. The removal of cortisol from the superfusion buffer resulted in a slow recovery of basal ACTH release and a recovery of the ACTH-releasing activities of urotensin I, CRF and sauvagine. These results are supportive of the view that urotensin I, or a urotensin I-like peptide, serves as a physiological regulator of ACTH release in teleost fishes.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D029845:Amphibian Proteins; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology*; D004357:Drug Synergism; D006054:Goldfish; D006854:Hydrocortisone / Q000494:pharmacology*; D036361:Peptide Hormones; D010455:Peptides / Q000494:pharmacology*; D010477:Perfusion; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D013997:Time Factors; D014579:Urotensins / Q000494:pharmacology*
D029845:Amphibian Proteins; D036361:Peptide Hormones; D010455:Peptides; D014579:Urotensins; C025727:sauvagine; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; C029676:urotensin I; D006854:Hydrocortisone