Linked Life Data

2541624

Source:http://linkedlifedata.com/resource/pubmed/id/2541624

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1989-6-16
pubmed:abstractText
Systemic hypoxia has been reported to inhibit selectively aldosterone secretion in vivo. The mechanism of this inhibition has not been elucidated. We hypothesized that decreased tissue PO2 directly inhibited aldosteronogenesis. To test this hypothesis, we exposed dispersed adrenocortical cells (90% glomerulosa/10% fasciculata) to decreased PO2 in vitro while simultaneously stimulating aldosterone secretion with angiotensin II, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dibutyryl cAMP) adrenocorticotropic hormone (ACTH)-(1-24), or progesterone. Decreasing buffer PO2 from approximately 150 to approximately 85 Torr significantly inhibited basal and angiotensin II, cAMP, progesterone, and ACTH-stimulated aldosterone secretion at all doses of secretagogue. Inhibition was largest for angiotensin II (55 +/- 9% inhibition at 1 microM) and cAMP (54 +/- 8% at 3 mM) and lowest for ACTH (24% at 100 nM) and basal aldosterone secretion (31 +/- 7%). This inhibition was reversed by returning the buffer PO2 to 150 Torr. Cortisol secretion was not significantly inhibited by decreased buffer PO2. We conclude that decreased buffer PO2 significantly inhibits aldosterone secretion in vitro, and this inhibition is reversible and specific. Hypoxia-induced inhibition of aldosterone secretion in vivo may be caused, at least in part, by a direct effect of low tissue PO2 within the adrenal cortex.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
256
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E640-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Low oxygen selectively inhibits aldosterone secretion from bovine adrenocortical cells in vitro.
pubmed:affiliation
Department of Medicine, St. Luke's Medical Center, Medical College of Wisconsin, Milwaukee 53215.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.