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Control of aldosterone release in vitro in the renin knockout rat
Author(s) -
Bruder Eric D,
Nunez Lizbeth,
Hoffman Matthew J,
Moreno Carol,
Raff Hershel
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.909.3
Subject(s) - zona glomerulosa , medicine , endocrinology , aldosterone , corticosterone , renin–angiotensin system , zona fasciculata , adrenal gland , angiotensin ii , in vitro , adrenal cortex , stimulation , chemistry , biology , hormone , biochemistry , blood pressure
There are local tissue renin‐angiotensin systems (RAS) throughout the body, in addition to the classic renal (peripheral) RAS that is responsible for generating plasma angiotensin II (AngII). An adrenocortical RAS may be involved in the control of aldosterone (Aldo) synthesis in the zona glomerulosa (ZG). In order to characterize the control of adrenal steroid production by a local RAS, we utilized adrenal glands from renin knockout (KO) rats and compared steroidogenesis in vitro to wild‐type (WT) controls. Adrenal capsules (ZG; Aldo production) and subcapsules (zona reticularis/fasciculata [ZFR]; corticosterone production) were separately dispersed, cell concentration was normalized, and cells studied in vitro (4 experiments). Basal and cAMP‐stimulated Aldo production was significantly reduced in renin KO ZG cells. Corticosterone production was not different between WT and KO ZFR cells. The reduction in Aldo from the ZG of the renin KO adrenal may be due to the absence of chronic stimulation of the ZG by circulating AngII or to a reduction in locally released AngII within the adrenal gland. Supported by NIH HL‐82798.