Preferred Label : Ion Channels in Vascular Endothelium Pathway;
NCIt related terms : Ion Channels and Their Functional Role in Vascular Endothelium;
Alternative definition : BIOCARTA: 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be outdated - see the DesignNote.);
NCIt note : 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/.;
Biocarta ID : h_raccPathway;
Origin ID : C39209;
UMLS CUI : C1517593;
Semantic type(s)
has_gene_product_element
pathway_has_gene_element