Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.
Angiotensin II stimulated 45Ca2+ release from bovine adrenal glomerulosa cells. It also decreased the influx of 45Ca2+ into glomerulosa cells. The effects were observed within 2 min of hormone addition and were blocked by Saralasin a competitive inhibitor of angiotensin. Des-Phe8-angiotensin II, a biologically inert analog, was inactive in this system. Angiotensin II also inhibited the influx of 133Ba2+ and 54Mn2+, whereas 51Cr6+ and 57Co2+ were unaffected. Alterations in 45Ca2+ fluxes were seen with concentrations of angiotensin that stimulate aldosterone biosynthesis in bovine glomerulosa cell preparations. These results suggest that calcium plays a key role in angiotensin-stimulated aldosteronogenesis.
D000302:Adrenal Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000450:Aldosterone / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002417:Cattle; D007700:Kinetics; D007811:Lanthanum / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology
D000804:Angiotensin II; D000450:Aldosterone; D007811:Lanthanum; D011188:Potassium; D002118:Calcium