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pubmed:abstractText |
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.
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