dc.creatorHyslop, S
dc.creatorde Nucci, G
dc.date1991
dc.date2015-11-27T12:19:30Z
dc.date2015-11-27T12:19:30Z
dc.date.accessioned2018-03-29T00:53:18Z
dc.date.available2018-03-29T00:53:18Z
dc.identifierWiener Klinische Wochenschrift. v. 103, n. 14, p. 422-34, 1991.
dc.identifier0043-5325
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/1926869
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194312
dc.identifier1926869
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294545
dc.descriptionEndothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) are co-released from endothelial cells by stimuli acting via membrane-bound receptors or via non-receptor mediated mechanisms. The receptor-mediated release of EDRF and PGI2 is calcium-dependent and seems to be under the negative feedback regulation of protein kinase C. Significant interactions between EDRF and PGI2 or between their respective second messengers within the endothelial cell have not yet been conclusively demonstrated. Furthermore, although EDRF and PGI2 synergize in the inhibition of platelet aggregation, there is little evidence for such synergism in smooth muscle relaxation. These observations indicate that EDRF and PGI2 release may be coupled primarily by their requirement for raised intracellular calcium levels and by their regulation through protein kinase C.
dc.description103
dc.description422-34
dc.languageeng
dc.relationWiener Klinische Wochenschrift
dc.relationWien. Klin. Wochenschr.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectCalcium
dc.subjectEndothelium, Vascular
dc.subjectEpoprostenol
dc.subjectHumans
dc.subjectMuscle, Smooth, Vascular
dc.subjectNitric Oxide
dc.subjectPlatelet Aggregation
dc.subjectThrombosis
dc.titleThe Mechanisms And Significance Of The Coupled Release Of Endothelium-derived Relaxing Factor (edrf) And Prostacyclin (pgi2) From Endothelial Cells.
dc.typeArtículos de revistas


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