FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2029557672> ?p ?o ?g. }

• W2029557672 endingPage "1174" @default.
• W2029557672 startingPage "1173" @default.
• W2029557672 abstract "Certain agonists are known to dilate cerebral arteries and/or arterioles by hyperpolarizing the endothelium through activation of endothelial intermediate-conductance calcium-activated K channels (IKCa or KCa3.1) alone or in combination with small-conductance calcium-activated K channels (SKCa or KCa2.X, most likely KCa2.3) (Faraci et al, 2004; Marrelli et al, 2003; McNeish et al, 2006; You et al, 1999). A major component of this dilatory mechanism involves spread of the endothelial hyperpolarization to the vascular smooth muscle (VSM) through myo-endothelial gap junctions (Bryan et al, 2005). This hyperpolarization relaxes VSM by reducing cytoplasmic Ca2+ through closing voltage-operated calcium channels that reside in the plasmalemma of VSM but not endothelium. Although traditionally known as endothelium-derived hyperpolarizing factor, a more appropriate term for this mechanism of dilation is endothelium-dependent hyperpolarization (EDH), as no ‘factor', per se, is transferred between cells (Bryan et al, 2005).Utilizing techniques that covered a spectrum from single-cell K+ currents to isolated pressurized parenchymal arterioles (PAs) to laser Doppler perfusion, a measure of cerebral blood flow (CBF), Hannah et al (this issue) now demonstrate that this EDH mechanism does not require receptor stimulation but is active in the basal state and is responsible for helping to maintain a resting CBF. Although it has been known that IKCa and SKCa are expressed by endothelium, this is the first time that K+ currents from these channels have been measured in freshly isolated endothelial cells from cerebral vessels and the first for any arteriole. Given the difficulty in obtaining single-cell currents in freshly isolated endothelium in general, the fact that these were from arterioles is impressive. More importantly, Hannah et al demonstrated that IKCa and SKCa contribute to the resting tone of PA and contribute significantly to resting CBF. Combined blockade of IKCa and SKCa decreased CBF by ∼15%, a response similar to that produced by the inhibition of NO. Whereas previous studies have demonstrated EDH as an important mechanism in isolated vessels, Hannah et al now show that it is an important mechanism in vivo during resting conditions.Several observations point to the fact that EDH is a major regulator of CBF: (1) EDH is more important than NO as a dilator mechanism in isolated PA upon activation of P2Y2 receptors (You et al, 1999); (2) EDH contributes to resting CBF and the resting tone of arterioles (Hannah et al, this issue) (Cipolla and Bullinger, 2008; Cipolla et al, 2009); (3) EDH is as important as NO in controlling resting CBF (Hannah et al, this issue); and (4) EDH dilations persist or are even upregulated in cerebral vessels, following a number of pathological states, when NO bioavailability is diminished (Cipolla and Bullinger, 2008; Cipolla et al, 2009; Golding et al, 2001; Marrelli et al, 1999; Prisby et al, 2006). Thus, EDH must be considered as a significant mechanism for the regulation of CBF and as a potential target for increasing CBF in pathological states where flow has been compromised. Certainly, more in vivo studies, similar to the one highlighted by this editorial, are needed to fully understand the role of EDH in the cerebral circulation." @default.
• W2029557672 created "2016-06-24" @default.
• W2029557672 creator A5046544080 @default.
• W2029557672 creator A5046974353 @default.
• W2029557672 date "2010-12-22" @default.
• W2029557672 modified "2023-10-16" @default.
• W2029557672 title "Endothelium-Dependent Hyperpolarization: Out of the Dish and into the Brain" @default.
• W2029557672 cites W1965763455 @default.
• W2029557672 cites W1978692031 @default.
• W2029557672 cites W1994244417 @default.
• W2029557672 cites W1996579798 @default.
• W2029557672 cites W1999779715 @default.
• W2029557672 cites W2024103448 @default.
• W2029557672 cites W2034617762 @default.
• W2029557672 cites W2048707852 @default.
• W2029557672 cites W2066190048 @default.
• W2029557672 doi "https://doi.org/10.1038/jcbfm.2010.221" @default.
• W2029557672 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3099633" @default.
• W2029557672 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21179071" @default.
• W2029557672 hasPublicationYear "2010" @default.
• W2029557672 type Work @default.
• W2029557672 sameAs 2029557672 @default.
• W2029557672 citedByCount "3" @default.
• W2029557672 countsByYear W20295576722012 @default.
• W2029557672 countsByYear W20295576722016 @default.
• W2029557672 countsByYear W20295576722017 @default.
• W2029557672 crossrefType "journal-article" @default.
• W2029557672 hasAuthorship W2029557672A5046544080 @default.
• W2029557672 hasAuthorship W2029557672A5046974353 @default.
• W2029557672 hasBestOaLocation W20295576722 @default.
• W2029557672 hasConcept C126322002 @default.
• W2029557672 hasConcept C131453863 @default.
• W2029557672 hasConcept C169760540 @default.
• W2029557672 hasConcept C185592680 @default.
• W2029557672 hasConcept C2776992346 @default.
• W2029557672 hasConcept C66974803 @default.
• W2029557672 hasConcept C71240020 @default.
• W2029557672 hasConcept C71924100 @default.
• W2029557672 hasConcept C86803240 @default.
• W2029557672 hasConceptScore W2029557672C126322002 @default.
• W2029557672 hasConceptScore W2029557672C131453863 @default.
• W2029557672 hasConceptScore W2029557672C169760540 @default.
• W2029557672 hasConceptScore W2029557672C185592680 @default.
• W2029557672 hasConceptScore W2029557672C2776992346 @default.
• W2029557672 hasConceptScore W2029557672C66974803 @default.
• W2029557672 hasConceptScore W2029557672C71240020 @default.
• W2029557672 hasConceptScore W2029557672C71924100 @default.
• W2029557672 hasConceptScore W2029557672C86803240 @default.
• W2029557672 hasIssue "5" @default.
• W2029557672 hasLocation W20295576721 @default.
• W2029557672 hasLocation W20295576722 @default.
• W2029557672 hasLocation W20295576723 @default.
• W2029557672 hasLocation W20295576724 @default.
• W2029557672 hasOpenAccess W2029557672 @default.
• W2029557672 hasPrimaryLocation W20295576721 @default.
• W2029557672 hasRelatedWork W143442218 @default.
• W2029557672 hasRelatedWork W2017299125 @default.
• W2029557672 hasRelatedWork W2034559055 @default.
• W2029557672 hasRelatedWork W2045736690 @default.
• W2029557672 hasRelatedWork W2069002240 @default.
• W2029557672 hasRelatedWork W2126945990 @default.
• W2029557672 hasRelatedWork W2202139434 @default.
• W2029557672 hasRelatedWork W2363650772 @default.
• W2029557672 hasRelatedWork W2748952813 @default.
• W2029557672 hasRelatedWork W2899084033 @default.
• W2029557672 hasVolume "31" @default.
• W2029557672 isParatext "false" @default.
• W2029557672 isRetracted "false" @default.
• W2029557672 magId "2029557672" @default.
• W2029557672 workType "article" @default.