Linked Life Data

11744017

Source:http://linkedlifedata.com/resource/pubmed/id/11744017

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-12-17
pubmed:abstractText
Oxygen (O(2)) tension is a major regulator of blood flow in the coronary circulation. Hypoxia can produce vasodilation through activation of ATP regulated K(+) (K(ATP)) channels in the myocyte membrane, which leads to hyperpolarization and closure of voltage-gated Ca(2+) channels. However, there are other O(2)-sensitive mechanisms intrinsic to the vascular smooth muscle since hypoxia can relax vessels precontracted with high extracellular K(+), a condition that prevents hyperpolarization following opening of K(+) channels. The objective of the present study was to determine whether inhibition of Ca(2+) influx through voltage-dependent channels participates in the response of coronary myocytes to hypoxia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-104
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Reduction of Ca(2+) channel activity by hypoxia in human and porcine coronary myocytes.
pubmed:affiliation
Laboratorio de Investigaciones Biomédicas, Edificio de Laboratorios, 2 planta, Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Avenida Manuel Siurot s/n, E-41013 Seville, Spain.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't