Linked Life Data

12364389

Source:http://linkedlifedata.com/resource/pubmed/id/12364389

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-10-4
pubmed:abstractText
Carbon monoxide (CO) is generated endogenously by the enzyme heme oxygenase. Although CO is a known vasodilator, cellular signaling mechanisms are poorly understood and are a source of controversy. The goal of the present study was to investigate mechanisms of CO dilation in porcine cerebral arterioles. Data indicate that exogenous or endogenously produced CO is a potent activator of large-conductance Ca2+-activated K+ (K(Ca)) channels and Ca2+ spark-induced transient K(Ca) currents in arteriole smooth muscle cells. In contrast, CO is a relatively poor activator of Ca2+ sparks. To understand the apparent discrepancy between potent effects on transient K(Ca) currents and weak effects on Ca2+ sparks, regulation of the coupling relationship between these events by CO was investigated. CO increased the percentage of Ca2+ sparks that activated a transient K(Ca) current (ie, the coupling ratio) from approximately 62% in the control condition to 100% and elevated the slope of the amplitude correlation between these events approximately 2.6-fold, indicating that Ca2+ sparks induced larger amplitude transient K(Ca) currents in the presence of CO. This signaling pathway for CO is physiologically relevant because ryanodine, a ryanodine-sensitive Ca2+ release channel blocker that inhibits Ca2+ sparks, abolished CO dilation of pial arterioles in vivo. Thus, CO dilates cerebral arterioles by priming K(Ca) channels for activation by Ca2+ sparks. This study presents a novel dilatory signaling pathway for CO in the cerebral circulation and appears to be the first demonstration [corrected] of a vasodilator that acts by increasing the effective coupling of Ca2+ sparks to K(Ca) channels.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
4
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
610-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12364389-Animals, pubmed-meshheading:12364389-Arterioles, pubmed-meshheading:12364389-Calcium Channel Blockers, pubmed-meshheading:12364389-Calcium Signaling, pubmed-meshheading:12364389-Carbon Monoxide, pubmed-meshheading:12364389-Cells, Cultured, pubmed-meshheading:12364389-Cerebral Arteries, pubmed-meshheading:12364389-Culture Techniques, pubmed-meshheading:12364389-Electric Conductivity, pubmed-meshheading:12364389-Heme, pubmed-meshheading:12364389-Kinetics, pubmed-meshheading:12364389-Lysine, pubmed-meshheading:12364389-Muscle, Smooth, Vascular, pubmed-meshheading:12364389-Potassium Channels, Calcium-Activated, pubmed-meshheading:12364389-Ryanodine, pubmed-meshheading:12364389-Ryanodine Receptor Calcium Release Channel, pubmed-meshheading:12364389-Signal Transduction, pubmed-meshheading:12364389-Swine, pubmed-meshheading:12364389-Vasodilation, pubmed-meshheading:12364389-Vasodilator Agents
pubmed:year
2002
pubmed:articleTitle
Carbon monoxide dilates cerebral arterioles by enhancing the coupling of Ca2+ sparks to Ca2+-activated K+ channels.
pubmed:affiliation
Department of Physiology, University of Tennessee Health Science Center, Memphis 38163, USA. jjaggar@physio1.utmem.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't