Key result
Urotensin-II concentration-dependently decreased basal corticosterone secretion from cultured rat adrenocortical cells, an effect abolished by the UT-R antagonist Palosuran.
Urotensin-II acts in an autocrine-paracrine manner to inhibit basal glucocorticoid secretion in the rat adrenal cortex via the UT-R receptor.
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Should not yet influence clinical adrenal management; hypothesis-generating for UT-R modulation of glucocorticoid secretion.
Urotensin-II (UII) is a potent hypertensive peptide, which has been recognized as an endogenous ligand of the G protein-coupled receptor (GPR)-14, now named UT-R. Real-time PCR demonstrated the expression of UII and UT-R mRNAs in both dispersed and in vitro cultured rat adrenocortical cells. UII concentration-dependently decreased basal, but not ACTH-stimulated, corticosterone secretion from cultured adrenocortical cells, and the effect was abolished by the UT-R antagonist Palosuran. UII did not affect the proliferation rate of cultured cells. Taken together, these findings suggest that UII may be included in the group of peptides (adrenomedullin, atrial natriuretic peptide, neurotensin and beacon), that, acting in an autocrine-paracrine manner, are involved in the inhibitory tuning of adrenocortical secretion.
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Albertin et al. (2006) studied this question. Urotensin-II vs. Control (baseline) cultures without any chemical was evaluated on Basal corticosterone secretion (p=<0.01). Urotensin-II concentration-dependently decreased basal corticosterone secretion from cultured rat adrenocortical cells, an effect abolished by the UT-R antagonist Palosuran.
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