Linked Life Data

15637296

Source:http://linkedlifedata.com/resource/pubmed/id/15637296

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-18
pubmed:abstractText
We hypothesized that shear stress stimulates the release of epoxyeicosatrienoic acids (EETs) from arteriolar endothelium, which directly hyperpolarize smooth muscle. To test this hypothesis, a perfusion system, consisting of two separate, serially connected chambers (A and B), was used. A donor vessel, isolated from gracilis muscle of female NO-deficient mice and rats, was cannulated in chamber A. In chamber B, an endothelium-denuded detector vessel isolated from mesentery of these animals was cannulated. In the presence of indomethacin, 5, 10, and 20 dyne/cm2 shear stress elicited dilation of donor vessels, followed by dilation of detector vessels. Changes in membrane potential of the detector vessel smooth muscle cells in response to the perfusate from 5 and 10 dyne/cm2 shear stress-stimulated donor vessels was also recorded (by approximately -12 to -15 and -20 to -30 mV, respectively). Exposing detector vessels to 30 mmol/L KCl or pretreating them with iberiotoxin abolished their hyperpolarization and dilation to the flow of perfusate. Pretreatment of donor vessels with PPOH, an inhibitor of cytochrome P-450/epoxygenase, eliminated dilator responses in both donor and detector vessels, as well as the hyperpolarization of detector vessels. GC-MS analysis showed increasing release of EETs into the perfusate collected from 1, 5, and 10 dyne/cm2 shear stress-stimulated arterioles, which was abolished by PPOH. Thus, EETs, released from endothelial cells of donor vessels stimulated with shear stress, hyperpolarize smooth muscle of downstream detector vessels, confirming their identity as endothelium-derived hyperpolarizing factors and suggesting that gap junctional communication may not be necessary for shear stress-stimulated EDHF-mediated vasodilation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
18
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
376-83
pubmed:dateRevised
2011-11-1
pubmed:meshHeading
pubmed-meshheading:15637296-8,11,14-Eicosatrienoic Acid, pubmed-meshheading:15637296-Animals, pubmed-meshheading:15637296-Blood Vessels, pubmed-meshheading:15637296-Culture Media, Conditioned, pubmed-meshheading:15637296-Diffusion Chambers, Culture, pubmed-meshheading:15637296-Endothelium, Vascular, pubmed-meshheading:15637296-Female, pubmed-meshheading:15637296-Indomethacin, pubmed-meshheading:15637296-Male, pubmed-meshheading:15637296-Membrane Potentials, pubmed-meshheading:15637296-Mesenteric Arteries, pubmed-meshheading:15637296-Mice, pubmed-meshheading:15637296-Muscle, Smooth, Vascular, pubmed-meshheading:15637296-Nitric Oxide, pubmed-meshheading:15637296-Nitric Oxide Synthase, pubmed-meshheading:15637296-Nitric Oxide Synthase Type II, pubmed-meshheading:15637296-Nitric Oxide Synthase Type III, pubmed-meshheading:15637296-Perfusion, pubmed-meshheading:15637296-Rats, pubmed-meshheading:15637296-Stress, Mechanical, pubmed-meshheading:15637296-Tissue Culture Techniques
pubmed:year
2005
pubmed:articleTitle
Epoxyeicosatrienoic acids are released to mediate shear stress-dependent hyperpolarization of arteriolar smooth muscle.
pubmed:affiliation
Department of Physiology, New York Medical College Valhalla, NY 10595. an_huang@nymc.edu.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural