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- NCIT_C39167 NCIT_NHC0 "C39167" @default.
- NCIT_C39167 NCIT_P106 "Functional Concept" @default.
- NCIT_C39167 NCIT_P108 "Nitric Oxide Pathway" @default.
- NCIT_C39167 NCIT_P207 "C1518332" @default.
- NCIT_C39167 NCIT_P216 "h_no1Pathway" @default.
- NCIT_C39167 NCIT_P325 "Nitric oxide (NO) has a number of important physiological actions in the cardiovascular system. In the heart, NO plays a role in keeping the vessels open via vasodilation and prevention of platelet aggregation. It also plays an important role in regulating the force and rate of contraction. In vivo NO is released by shear stress of ligands that increase intracellular Ca2+ in endothelial cells. The increased intracellular Ca2+ activates nitric oxide synthase III (NOSIII) by promoting the binding of Ca/Calmodulin to the enzyme. NOSIII, which is resident in the Golgi complex, is transported together with caveolin-1 to the caveolae at the plasma membrane via vesicles. Shear stress signals via a potassium channel and the cytoskeleton, which results in tyrosine phosphorylation of specific proteins, activation of phosphatidylinositol 3-kinase, and subsequently in activation of Akt kinase. Akt activation by shear stress, but also by VEGF, activates NOSIII by serine phosphorylation, which increases the affinity of NOSIII for calmodulin. After agonist binding at the plasma membrane, NOSIII-activating receptors translocate to caveolae. VEGF receptor signals via its tyrosine kinase domain. Furthermore, agonist receptors activate calcium channels of the endoplasmic reticulum (ER) via phospholipase C and inositol 1,4,5-trisphosphate. This calcium flux induces binding of calmodulin to NOSIII, whereas the NOSIII-caveolin-1 interaction is disrupted. At the same time, NOSIII is translocated into the cytosol. On binding of calmodulin, NOSIII generates NO, is enhanced by the interaction with Hsp90. Once activated, NOSIII catabolizes L-arginine to NO, which diffuses out of the cell. NO stimulates guanylate (G-) cyclase and increases cGMP levels. cGMP activates cGMP-dependent protein kinase (PKG), cGMP-inhibited phosphodiesterase (PDEIII), and cGMP-stimulated phosphodiesterase (PDEII). PKG may reduce the force and rate of contraction, possibly by phosphorylating troponin I or by phosphorylating phospholamban. PDEIII is inhibited by the increases in cGMP brought about by NO. This may result in an increase in cAMP and cAMP-dependent protein kinase (PKA). PKA in turn activates Ca2+ channels, countering the effects of PKG. In contrast, cGMP may stimulate PDEII, reduce cAMP levels and PKA activity, and thereby reduce Ca2+ channel activity. (This definition may be outdated - see the DesignNote.)" @default.
- NCIT_C39167 NCIT_P366 "Nitric_Oxide_Pathway" @default.
- NCIT_C39167 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_C39167 normalizedInformationContent "75.267234140859458" @default.
- NCIT_C39167 referenceCount "42" @default.
- NCIT_C39167 hasExactSynonym "Actions of Nitric Oxide in the Heart" @default.
- NCIT_C39167 hasExactSynonym "Nitric Oxide Pathway" @default.
- NCIT_C39167 type Class @default.
- NCIT_C39167 isDefinedBy ncit.owl @default.
- NCIT_C39167 label "Nitric Oxide Pathway" @default.
- NCIT_C39167 subClassOf NCIT_C17132 @default.
- NCIT_C39167 subClassOf NCIT_C20633 @default.
- NCIT_C39167 subClassOf NCIT_C39167 @default.