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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 1
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pubmed:dateCreated |
1989-2-21
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pubmed:abstractText |
The sustained aldosterone secretory response to angiotensin II (ANG II) depends on receptor-mediated increases in membrane diglyceride (DG) and an increase in calcium influx rate. These signals serve to activate membrane-associated protein kinase C (PKC) and result in enhanced phosphorylation of a unique set of proteins. These events can be mimicked by the addition of a phorbol ester, 12-O-tetra decanoyl phorbol 13-acetate (TPA), and a calcium ionophore, A23187, that bypass the initial receptor-associated events. We studied the inhibitory action of atrial natriuretic peptide (4-28 hANP) on the sustained secretory response to ANG II in isolated bovine adrenal glomerulosa cells. Although 10 nM ANP inhibited aldosterone secretion, it did not significantly alter the ANG II-elicited rise in 45Ca2+ influx rate [control (CON): 0.44 +/- 0.06; ANG II: 1.11 +/- 0.12 (P less than 0.001); ANG II + ANP: 1.18 +/- 0.14], the steady-state level of aequorin luminescence [intracellular [Ca2+] ([Ca2+]i)], or the rise in cellular DG content [CON: 0.132 +/- 0.01; ANG II: 0.194 +/- 0.01 (P less than 0.005); ANG II + ANP: 0.202 +/- 0.01 nmol/10(6) cells]. IN addition, ANP was able to inhibit aldosterone secretion stimulated by the combined addition of A23187 + TPA. When protein phosphorylation in the ANP-inhibited cells was evaluated, ANG II-induced protein phosphorylation events were preserved. In contrast to the effect of ANP, the calcium channel blocker nitrendipine abolished the ANG II-induced rise in 45Ca2+ influx rate, reduced the steady-state level of [Ca2+]i, and returned the phosphoproteins to their control states.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aequorin,
http://linkedlifedata.com/resource/pubmed/chemical/Aldosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Diglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/atrial natriuretic factor (4-28)
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
256
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C89-95
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:2521426-Aequorin,
pubmed-meshheading:2521426-Aldosterone,
pubmed-meshheading:2521426-Angiotensin II,
pubmed-meshheading:2521426-Animals,
pubmed-meshheading:2521426-Atrial Natriuretic Factor,
pubmed-meshheading:2521426-Calcimycin,
pubmed-meshheading:2521426-Calcium,
pubmed-meshheading:2521426-Cattle,
pubmed-meshheading:2521426-Cell Membrane,
pubmed-meshheading:2521426-Diglycerides,
pubmed-meshheading:2521426-Luminescent Measurements,
pubmed-meshheading:2521426-Peptide Fragments,
pubmed-meshheading:2521426-Phosphoproteins,
pubmed-meshheading:2521426-Phosphorylation,
pubmed-meshheading:2521426-Protein Kinase C,
pubmed-meshheading:2521426-Second Messenger Systems,
pubmed-meshheading:2521426-Tetradecanoylphorbol Acetate,
pubmed-meshheading:2521426-Zona Glomerulosa
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pubmed:year |
1989
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pubmed:articleTitle |
Effect of ANP on sustained aldosterone secretion stimulated by angiotensin II.
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pubmed:affiliation |
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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