Potassium fluxes in bovine adrenal cells during adrenocorticotropin stimulation.
Active (ouabain-sensitive) and passive (ouabain-insensitive) fluxes of 43K were measured in isolated bovine zona fasciculata/reticularis cells. ACTH inhibited passive influx in a dose-dependent manner and, at a concentration that maximally stimulated steroidogenesis (10(-8) M), also inhibited passive efflux. ACTH did not affect active potassium transport. Angiotensin II (10(-6) M) and cAMP (10(-2) M) inhibited passive influx to the same extent as did 10(-8) M ACTH. Angiotensin II (10(-6) M) also reduced active potassium uptake, although this did not appear to be related to changes in cortisol biosynthesis. Increases in cortisol synthesis by ouabain-treated cells in response to angiotensin II and ACTH were proportional to decreases in potassium influx. The addition of cortisol (1 microgram/ml) to cells slightly reduced passive potassium uptake, but not to the same extent as did 10(-8) M ACTH. Frusemide, an inhibitor of passive sodium/potassium cotransport, did not wholly abolish the effects of ACTH on potassium influx. These changes in flux are probably related to electrophysiological changes in membrane potential. Their significance in the regulation of ACTH actions has yet to be determined.
Kenyon
C J
CJ
Young
J
J
Fraser
R
R
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002417:Cattle; D002463:Cell Membrane Permeability / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005665:Furosemide / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology; D066298:In Vitro Techniques; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*
D000804:Angiotensin II; D010042:Ouabain; D003994:Bucladesine; D005665:Furosemide; D000324:Adrenocorticotropic Hormone; D011188:Potassium; D006854:Hydrocortisone