{"title":"内皮:血管信息交换","authors":"R. Wei, S. Lunn, S. Gust, P. Kerr, F. Plane","doi":"10.5772/INTECHOPEN.79897","DOIUrl":null,"url":null,"abstract":"Maintenance of adequate blood flow to tissues and organs requires that endothelial cells dynamically respond in a stimulus-specific manner to elicit appropriate changes in smooth muscle contractility and thus, arterial diameter. Endothelial cells can be stimu- lated directly by increases in blood flow and by humoral factors acting on surface receptors, as well as through flux of second messengers from smooth muscle cells activated by release of neurotransmitters from perivascular nerves. The ability of endothelial cells to generate stimulus-specific responses to these diverse inputs is facilitated by organization of ion channels and signaling proteins into microdomains that permit finely-tuned, spatially-restricted Ca 2+ events to differentially activate key effectors such as nitric oxide (NO) synthase and Ca 2+ -activated K + (K Ca ) channels. NO is a diffusible mediator which acts locally to cause vasodilation. Opening of K Ca channels causes hyperpolarization of the endothelial membrane potential which spreads to surrounding smooth muscle cells to also cause local vasodilation. However, once initiated, hyperpolarization also spreads longitudinally through the endothelium to effect coordinated changes in blood flow within multiple arterial segments. Thus, the signaling pathways activated by a particular stimulus determine whether it ’ s effects on arterial diameter are localized or can impact blood flow at the level of the vascular bed. by increases in shear stress. Shear stress-evoked Ca 2+ influx through TRPV4 channels on the luminal surface of endothelial cells leads to spatially-restricted Ca 2+ sparklets within a signaling microdomain to selectively activate SK ca channels and endothelial NOS (eNOS).","PeriodicalId":9411,"journal":{"name":"Calcium and Signal Transduction","volume":"57 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"The Endothelium: The Vascular Information Exchange\",\"authors\":\"R. Wei, S. Lunn, S. Gust, P. Kerr, F. Plane\",\"doi\":\"10.5772/INTECHOPEN.79897\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Maintenance of adequate blood flow to tissues and organs requires that endothelial cells dynamically respond in a stimulus-specific manner to elicit appropriate changes in smooth muscle contractility and thus, arterial diameter. Endothelial cells can be stimu- lated directly by increases in blood flow and by humoral factors acting on surface receptors, as well as through flux of second messengers from smooth muscle cells activated by release of neurotransmitters from perivascular nerves. The ability of endothelial cells to generate stimulus-specific responses to these diverse inputs is facilitated by organization of ion channels and signaling proteins into microdomains that permit finely-tuned, spatially-restricted Ca 2+ events to differentially activate key effectors such as nitric oxide (NO) synthase and Ca 2+ -activated K + (K Ca ) channels. NO is a diffusible mediator which acts locally to cause vasodilation. Opening of K Ca channels causes hyperpolarization of the endothelial membrane potential which spreads to surrounding smooth muscle cells to also cause local vasodilation. However, once initiated, hyperpolarization also spreads longitudinally through the endothelium to effect coordinated changes in blood flow within multiple arterial segments. Thus, the signaling pathways activated by a particular stimulus determine whether it ’ s effects on arterial diameter are localized or can impact blood flow at the level of the vascular bed. by increases in shear stress. Shear stress-evoked Ca 2+ influx through TRPV4 channels on the luminal surface of endothelial cells leads to spatially-restricted Ca 2+ sparklets within a signaling microdomain to selectively activate SK ca channels and endothelial NOS (eNOS).\",\"PeriodicalId\":9411,\"journal\":{\"name\":\"Calcium and Signal Transduction\",\"volume\":\"57 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-10-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Calcium and Signal Transduction\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5772/INTECHOPEN.79897\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Calcium and Signal Transduction","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.79897","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Endothelium: The Vascular Information Exchange
Maintenance of adequate blood flow to tissues and organs requires that endothelial cells dynamically respond in a stimulus-specific manner to elicit appropriate changes in smooth muscle contractility and thus, arterial diameter. Endothelial cells can be stimu- lated directly by increases in blood flow and by humoral factors acting on surface receptors, as well as through flux of second messengers from smooth muscle cells activated by release of neurotransmitters from perivascular nerves. The ability of endothelial cells to generate stimulus-specific responses to these diverse inputs is facilitated by organization of ion channels and signaling proteins into microdomains that permit finely-tuned, spatially-restricted Ca 2+ events to differentially activate key effectors such as nitric oxide (NO) synthase and Ca 2+ -activated K + (K Ca ) channels. NO is a diffusible mediator which acts locally to cause vasodilation. Opening of K Ca channels causes hyperpolarization of the endothelial membrane potential which spreads to surrounding smooth muscle cells to also cause local vasodilation. However, once initiated, hyperpolarization also spreads longitudinally through the endothelium to effect coordinated changes in blood flow within multiple arterial segments. Thus, the signaling pathways activated by a particular stimulus determine whether it ’ s effects on arterial diameter are localized or can impact blood flow at the level of the vascular bed. by increases in shear stress. Shear stress-evoked Ca 2+ influx through TRPV4 channels on the luminal surface of endothelial cells leads to spatially-restricted Ca 2+ sparklets within a signaling microdomain to selectively activate SK ca channels and endothelial NOS (eNOS).