Adrenocorticotropin regulates angiotensin II receptors in bovine adrenal cells in vitro.
The role of ACTH-(1-24) on angiotensin II receptors has been studied in bovine adrenal glomerulosa cells in primary culture. Angiotensin II receptors were measured in cells pretreated or not by ACTH-(1-24) on day 4 of culture. ACTH-(1-24) decreased angiotensin II binding sites in a time and a dose-dependent manner. After 24 hours of treatment the minimal effective dose of ACTH-(1-24) was 10(-11)M and the maximal effect was obtained with 10(-8)M. Moreover, ACTH-(1-24) 10(-8)M decreased significantly angiotensin II receptors after 6 hours of treatment. Scatchard plot analysis showed that ACTH-(1-24) treatment did not modify the affinity of angiotensin II receptors (Ka = 0.42 and 0.44 X 10(9)M-1 in control and treated cells respectively) but reduced by about half the number of angiotensin II sites per cell. Like ACTH-(1-24), 8-Bromo-cAMP, forskolin and cholera toxin decreased angiotensin II receptors. Factors such as prolactin, somatostatin, ACTH-(11-24) and dopamine which are bound to adrenal membranes without increasing cAMP production had no effect. In conclusion, these studies in vitro demonstrate for the first time that ACTH decreases angiotensin II receptors by a direct mechanism acting on glomerulosa cells, and they also suggest that this effect could be mediated by cAMP.
D000311:Adrenal Glands / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D002772:Cholera Toxin / Q000494:pharmacology; D005576:Colforsin; D000242:Cyclic AMP / Q000096:biosynthesis / Q000502:physiology; D004224:Diterpenes / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000187:drug effects*; D011956:Receptors, Cell Surface / Q000187:drug effects*
D004224:Diterpenes; D011945:Receptors, Angiotensin; D011956:Receptors, Cell Surface; D005576:Colforsin; D000324:Adrenocorticotropic Hormone; D002772:Cholera Toxin; D000242:Cyclic AMP