Linked Life Data

1311716

Source:http://linkedlifedata.com/resource/pubmed/id/1311716

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1992-4-7
pubmed:abstractText
Stimulation of the release of endothelium-derived relaxing factor (EDRF) in the kidney has been shown to result in natriuresis without affecting glomerular filtration rate. This may be due to EDRF directly regulating solute transport in the cortical collecting duct (CCD). To test this hypothesis, we measured the effect of bradykinin (Bk) or acetylcholine (Ach) on short-circuit current (Isc; a measure of active transport) in a CCD cell line (M-1), in the presence or absence of cow pulmonary artery endothelial (CPAE) cells. 10(-9) M Bk or 10(-7) M Ach had no effect on M-1 Isc in which CPAE cells were absent. The addition of CPAE cells to M-1 cells also did not affect M-1 Isc. On the other hand, when 10(-9) M Bk or 10(-7) M Ach were added to M-1 cells in the presence of CPAE cells, Isc decreased from 43 +/- 4.5 to 26 +/- 4 and 64 +/- 9 to 33 +/- 4 microA/cm2, respectively (P less than 0.001). Nitroarginine (N-Arg, 10(-4) M), a competitive inhibitor of EDRF production, blocked the inhibition in M-1 Isc due to both agonists. Since cGMP is the second messenger of EDRF in vascular smooth muscle, we measured the effects of Bk on cGMP production in M-1 cells in the presence and absence of CPAE cells. Bk increased cGMP content in M-1 cells in the presence of CPAE cells from 33 +/- 3.4 to 132 +/- 11.7 fmol/10(6) M-1 cells (P less than 0.001). When cultures of M-1 and CPAE cells were treated with N-Arg and challenged with Bk, Bk's effect on cGMP was partially blocked (61.4 +/- 12 fmol/10(-6) M-1 cells; NS). These data suggest that EDRF inhibits transport and increases cGMP content in M-1 cells.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-1654478, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2022735, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2043304, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2110626, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2140836, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2154125, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2167016, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2328404, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2347626, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2379949, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2435176, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2451132, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2458385, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2498003, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2521430, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2545495, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2661425, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2844855, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-2983068, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-3131684, http://linkedlifedata.com/resource/pubmed/commentcorrection/1311716-3495737
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
761-5
pubmed:dateRevised
2010-9-7
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Endothelium-derived relaxing factor inhibits transport and increases cGMP content in cultured mouse cortical collecting duct cells.
pubmed:affiliation
Department of Medicine, Henry Ford Hospital, Detroit, Michigan 48202.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.