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Mol Cell Endocrinol. 1991 Oct;81(1-3):33-41.

Angiotensin-II activation of cAMP and corticosterone production in bovine adrenocortical cells: effects of nonpeptide angiotensin-II antagonists.

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Department of Obstetrics and Gynecology and Biochemistry, University of Texas, Southwestern Medical Center, Dallas 75235-9032.


The ability of angiotensin-II (A-II) to increase cAMP production in adrenocortical cells is not widely accepted due to numerous conflicting reports. The recent observation that rat adrenal cells exhibit multiple subtypes of A-II receptors raises the possibility that a specific subtype could be responsible for controlling cAMP stimulation. In the present study we characterize in detail the effects of A-II on cAMP production in bovine adrenocortical zona fasciculata cells (BAC) cells and determined which A-II receptor subtype is responsible for stimulating both cAMP production and steroidogenesis. A-II (100 nM) increased the medium content of cAMP by 5- to 10-fold. The magnitude of A-II stimulation, while significant, was considerably less than that observed following treatment with ACTH (100 nM) (10-fold vs. 500-fold). The A-II stimulation of cAMP was both concentration and time dependent with a significant increase in cAMP observed in the presence of 1 nM A-II and a maximal response observed using 100 nM A-II. Stimulation was also seen using the decapeptide, A-I, and the heptapeptide, A-III. Of the angiotensin analogues tested, the order of potency was A-II greater than A-III greater than A-I. The A-II antagonist, [Sar1, Ala8]-A-II (saralasin), reversed the stimulatory effect of A-II. The superior potency of A-II and the ability of saralasin to inhibit cAMP production suggest a specific receptor mediated mechanism.(ABSTRACT TRUNCATED AT 250 WORDS).

[Indexed for MEDLINE]

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