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- NCIT_C39209 NCIT_NHC0 "C39209" @default.
- NCIT_C39209 NCIT_P106 "Functional Concept" @default.
- NCIT_C39209 NCIT_P108 "Ion Channels in Vascular Endothelium Pathway" @default.
- NCIT_C39209 NCIT_P207 "C1517593" @default.
- NCIT_C39209 NCIT_P216 "h_raccPathway" @default.
- NCIT_C39209 NCIT_P325 "Endothelial cells (EC) form a multifunctional signal-transducing surface that performs different tasks dependent on its localization in the vessel tree. Arterial EC provide a pathway for delivery of oxygen from blood to tissue. They modulate the tone of vascular smooth muscle cells, which in turn controls blood pressure and blood flow by adjusting the caliber of arteries and arterioles. In the microvascular bed, EC regulate the permeation of various metabolites, macromolecules, and gases, as well as autocrine and paracrine factors and are involved in the regulation of cell nutrition. In all vessel types, EC are involved in blood coagulation, control of the transport between blood and tissue, movement of cells adhering to EC, wound healing, and angiogenesis. Other functions require an active response of EC to various signals of mechanical, chemical, or neuronal nature. This signal transduction is impaired during vessel disease (arteriosclerosis) and injury, inflammation, or hemodynamic disturbances (hypertension). The role of ion channels in the transduction of these signals into cellular responses is still a matter of debate and has received substantial attention only in the last few years. Our current knowledge is limited to effects of ion channels on fast endothelial responses, these channels being mainly essential for the regulation of Ca2+ signaling. Here we illustrate the negative feedback of cyclic nucleotides (CNG)-induced membrane depolarization on Ca2+ entry. Ca2+ entry via receptor-activated cation channels (RACC) and/or store-operated or capacitative (SOC) elevates [Ca2+]i and stimulates endothelial nitric oxide synthase (eNOS). The subsequent activation of soluble guanylate cyclase (sGC) increases cGMP. cGMP and cAMP, via agonist activation of G protein-coupled receptors (GPCRs), Gs, and adenylate cyclase (AC), activate CNG and/or nonselective cation channels (HCN) channels, which induce membrane depolarization. This depolarization exerts a negative feedback on Ca2+ entry via RACC/SOC. In addition, a feedback inhibition of Ca2+ entry channels via activation of PKG has been described. (This definition may be outdated - see the DesignNote.)" @default.
- NCIT_C39209 NCIT_P366 "Ion_Channels_in_Vascular_Endothelium_Pathway" @default.
- NCIT_C39209 NCIT_P98 "The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA Definition might be outdated or inaccurate. Please see the Terms and Conditions for Use at http://www.biocarta.com/." @default.
- NCIT_C39209 normalizedInformationContent "77.950262499983424" @default.
- NCIT_C39209 referenceCount "28" @default.
- NCIT_C39209 hasExactSynonym "Ion Channels and Their Functional Role in Vascular Endothelium" @default.
- NCIT_C39209 hasExactSynonym "Ion Channels in Vascular Endothelium Pathway" @default.
- NCIT_C39209 type Class @default.
- NCIT_C39209 isDefinedBy ncit.owl @default.
- NCIT_C39209 label "Ion Channels in Vascular Endothelium Pathway" @default.
- NCIT_C39209 subClassOf NCIT_C19779 @default.
- NCIT_C39209 subClassOf NCIT_C20633 @default.
- NCIT_C39209 subClassOf NCIT_C39209 @default.
- NCIT_C39209 subClassOf NCIT_C91822 @default.