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Calcium signals that determine vascular resistance

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dc.contributor.authorOttolini, Matteo-
dc.contributor.authorHong, Kwangseok-
dc.contributor.authorSonkusare, Swapnil K.-
dc.date.accessioned2021-06-18T07:24:00Z-
dc.date.available2021-06-18T07:24:00Z-
dc.date.issued2019-09-
dc.identifier.issn1939-5094-
dc.identifier.issn1939-005X-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/44702-
dc.description.abstractSmall arteries in the body control vascular resistance, and therefore, blood pressure and blood flow. Endothelial and smooth muscle cells in the arterial walls respond to various stimuli by altering the vascular resistance on a moment to moment basis. Smooth muscle cells can directly influence arterial diameter by contracting or relaxing, whereas endothelial cells that line the inner walls of the arteries modulate the contractile state of surrounding smooth muscle cells. Cytosolic calcium is a key driver of endothelial and smooth muscle cell functions. Cytosolic calcium can be increased either by calcium release from intracellular stores through IP3 or ryanodine receptors, or the influx of extracellular calcium through ion channels at the cell membrane. Depending on the cell type, spatial localization, source of a calcium signal, and the calcium-sensitive target activated, a particular calcium signal can dilate or constrict the arteries. Calcium signals in the vasculature can be classified into several types based on their source, kinetics, and spatial and temporal properties. The calcium signaling mechanisms in smooth muscle and endothelial cells have been extensively studied in the native or freshly isolated cells, therefore, this review is limited to the discussions of studies in native or freshly isolated cells. This article is categorized under: Biological Mechanisms > Cell Signaling Laboratory Methods and Technologies > Imaging Models of Systems Properties and Processes > Mechanistic Models-
dc.language영어-
dc.language.isoENG-
dc.publisherWILEY-
dc.titleCalcium signals that determine vascular resistance-
dc.typeArticle-
dc.identifier.doi10.1002/wsbm.1448-
dc.identifier.bibliographicCitationWILEY INTERDISCIPLINARY REVIEWS-SYSTEMS BIOLOGY AND MEDICINE, v.11, no.5-
dc.description.isOpenAccessN-
dc.identifier.wosid000480289400004-
dc.identifier.scopusid2-s2.0-85069670686-
dc.citation.number5-
dc.citation.titleWILEY INTERDISCIPLINARY REVIEWS-SYSTEMS BIOLOGY AND MEDICINE-
dc.citation.volume11-
dc.type.docTypeArticle-
dc.publisher.location미국-
dc.subject.keywordAuthorcalcium signaling-
dc.subject.keywordAuthorendothelium-
dc.subject.keywordAuthorion channels-
dc.subject.keywordAuthormicrocirculation-
dc.subject.keywordAuthorvascular smooth muscle-
dc.subject.keywordPlusARTERIAL SMOOTH-MUSCLE-
dc.subject.keywordPlusMYOENDOTHELIAL GAP-JUNCTIONS-
dc.subject.keywordPlusINOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR-
dc.subject.keywordPlusCATION CHANNEL TRPV4-
dc.subject.keywordPlusOPERATED CA2+ ENTRY-
dc.subject.keywordPlusPROTEIN-KINASE-C-
dc.subject.keywordPlusCA2+-ACTIVATED K+ CHANNELS-
dc.subject.keywordPlusCANONICAL TYPE-3 CHANNELS-
dc.subject.keywordPlusHAMSTER FEED ARTERIES-
dc.subject.keywordPlusPOTENTIAL VANILLOID 1-
dc.relation.journalResearchAreaResearch & Experimental Medicine-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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