title: Angiotensin II inhibits K(+)-induced Ca2+ signal generation in rat adrenal glomerulosa cells.
abstract: The Ca2(+)-mobilizing hormone angiotensin II (AII) dose-dependently inhibited the K(+)-induced sustained increase of cytoplasmic Ca2+ concentration in adrenal glomerulosa cells and caused a rapid decrease of cytoplasmic Ca2+ when added to cells already stimulated with K+. These effects of AII on the K(+)-induced Ca2+ signal were mimicked, although less effectively, by other Ca2(+)-mobilizing agonists such as [Arg8]vasopressin (AVP) and thapsigargin. Phorbol esters did not show such effects, nor did corticotropin (ACTH), a secretagogue acting via cyclic AMP. The K(+)-stimulated initial 45Ca2+ uptake, a measure of Ca2+ entry into glomerulosa cells, was also prevented by AII pretreatment, and was inhibited by AVP, but not by ACTH. The stimulatory effect of K+ on aldosterone production, however, was not inhibited by AII, and the AII-induced aldosterone production was further increased by increasing K+. These data indicate that AII is able to inhibit static increases in cytoplasmic Ca2+ by inhibiting Ca2+ entry through voltage-sensitive Ca2+ channels and, possibly, by activating Ca2+ extrusion from the cells. It is also concluded that the Ca2+ signal evoked by AII is very efficient in stimulating hormone secretion, and the secretory response of the cells becomes more sensitive to any further increase of Ca2+ entry through voltage-sensitive Ca2+ channels.
authors.affiliation: Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary.
authors.forename: T
authors.initials: T
authors.lastname: Balla
authors.forename: Z
authors.initials: Z
authors.lastname: Holló
authors.forename: P
authors.initials: P
authors.lastname: Várnai
authors.forename: A
authors.initials: A
authors.lastname: Spät
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000450:Aldosterone / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D000242:Cyclic AMP / Q000494:pharmacology; D003593:Cytoplasm / Q000378:metabolism; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013729:Terpenes / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D019284:Thapsigargin; D015384:Zona Glomerulosa / Q000187:drug effects / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D013729:Terpenes; D000804:Angiotensin II; D001127:Arginine Vasopressin; D000450:Aldosterone; D019284:Thapsigargin; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D013755:Tetradecanoylphorbol Acetate; D011188:Potassium; D002118:Calcium