Linked Life Data

9426302

Source:http://linkedlifedata.com/resource/pubmed/id/9426302

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-2-26
pubmed:abstractText
Nitric oxide (NO) has been implicated as a modulator of the vascular effects of angiotensin II (ANG II) in the kidney. We used a NO-sensitive microelectrode to study the effect of ANG II on NO release, and to determine the effect of selective inhibition of the ANG II subtype I receptor (AT1) with losartan (LOS) and candesartan (CAN). NO release from isolated and perfused renal resistance arteries was measured with a porphyrin-electroplated, carbon fiber. The vessels were microdissected from isolated perfused rat kidneys and perfused at constant flow and pressure in vitro. The NO-electrode was placed inside the glass collection cannula to measure vessel effluent NO concentration. ANG II stimulated NO release in a dose-dependent fashion: 0.1 nM, 10 nM and 1000 nM ANG II increased NO-oxidation current by 85+/-18 pA (n = 11), 148+/-22 pA (n = 11), and 193+/-29 pA (n = 11), respectively. These currents correspond to changes in effluent NO concentration of 3.4+/-0.5 nM, 6.1+/-1.1 nM, and 8.2+/-1.3 nM, respectively. Neither LOS (1 muM) nor CAN (1 nM) significantly affected basal NO production, but both AT1-receptor blockers markedly blunted NO release in response to ANG II (10 nM): 77+/-6% inhibition with LOS (n = 8) and 63+/-9% with CAN (n = 8). These results are the first to demonstrate that ANG II stimulates NO release in isolated renal resistance arteries, and that ANG II-induced NO release is blunted by simultaneous AT1-receptor blockade. Our findings suggest that endothelium-dependent modulation of ANG II-induced vasoconstriction in renal resistance arteries is mediated, at least in part, by AT1-receptor-dependent NO release.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
435
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
432-4
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9426302-Angiotensin II, pubmed-meshheading:9426302-Angiotensin Receptor Antagonists, pubmed-meshheading:9426302-Animals, pubmed-meshheading:9426302-Benzimidazoles, pubmed-meshheading:9426302-Biphenyl Compounds, pubmed-meshheading:9426302-Electric Conductivity, pubmed-meshheading:9426302-Endothelium, Vascular, pubmed-meshheading:9426302-Losartan, pubmed-meshheading:9426302-Male, pubmed-meshheading:9426302-Microelectrodes, pubmed-meshheading:9426302-Nitric Oxide, pubmed-meshheading:9426302-Oxidation-Reduction, pubmed-meshheading:9426302-Rats, pubmed-meshheading:9426302-Rats, Sprague-Dawley, pubmed-meshheading:9426302-Receptor, Angiotensin, Type 1, pubmed-meshheading:9426302-Receptor, Angiotensin, Type 2, pubmed-meshheading:9426302-Receptors, Angiotensin, pubmed-meshheading:9426302-Renal Artery, pubmed-meshheading:9426302-Tetrazoles, pubmed-meshheading:9426302-Vascular Resistance
pubmed:year
1998
pubmed:articleTitle
Angiotensin-II stimulates nitric oxide release in isolated perfused renal resistance arteries.
pubmed:affiliation
Department of Physiology, Göteborg University, S-41390 Göteborg, Sweden.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't