Advanced search
Start date
Betweenand

Venous endothelial factors: influence of angiotensin II and endothelin-1

Abstract

Endothelial cells play a key role throughout the circulation for modulating vascular function by the generation of Endothelium-Derived Relaxing Factors (EDRFs) represented by nitric oxide, prostacyclin and endothelium-derived hyperpolarizing factor, and Endothelium-Derived Constricting Factors (EDCFs), represented by prostaglandin H2 and thromboxane A2, reactive oxygen species, and the peptides angiotensin II (Ang II) and endothelin-1 (ET-1). Studies directed to the production of EDRFs and EDCFs in venous beds are scarce, and little is known about the peculiarities of endothelial physiology in distinct venous territories such as the vena cava and portal vein. Furthermore, it is known that the actions of Ang II and ET-1 in these beds are effectively modulated by the endothelial cell, however, important aspects of this modulation remain unknown, particularly in levels of cellular signaling. Considering that Ang II and ET-1 (and respective receptors) are very important pharmacological targets in the cardiocirculatory therapy adopted in various pathological situations, the refined understanding of these issues presents timely and relevant. Thus, this project proposes to examine important aspects of the endothelial physiology, using primary cultures of venous endothelial cells. The central goal is the identification, quantification and characterization of the main EDRFs and EDCFs produced by venous endothelium, observing simultaneously the influence of Ang II and ET-1 on the endothelial function in the portal vein and inferior vena cava of rats. (AU)

Articles published in Agência FAPESP Newsletter about the research grant:
Articles published in other media outlets (0 total):
More itemsLess items
VEICULO: TITULO (DATA)
VEICULO: TITULO (DATA)

Scientific publications (5)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
BALBINO, ALEKSANDRO M.; SILVA, MARINA M.; AZEVEDO, GABRIELA A.; GIL, NOEMI L.; FERREIRA, RENAIDE R.; DOS SANTOS, LEILA A.; GASPARIN, REBECA M.; FERNANDES, LILIAM; LANDGRAF, MARISTELLA A.; LANDGRAF, RICHARDT G.. Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide. Mediators of Inflammation, v. 2018, p. 11-pg., . (14/18760-4, 12/51104-8, 17/02042-3, 10/01404-0)
TRINDADE, MARCIO RENATO; REIS ASSUNCAO, HENRIQUE CHARLANTI; TORRES, TATHIANY CORTEZE; BERTOLINO, JESSICA SILVA; FERNANDES, LILIAM. Venous endothelium reactivity to Angiotensin II: A study in primary endothelial cultures of rat vena cava and portal vein. Experimental Cell Research, v. 362, n. 1, p. 188-194, . (14/18760-4, 15/23584-3)
BALBINO, ALEKSANDRO M.; SILVA, MARINA M.; AZEVEDO, GABRIELA A.; GIL, NOEMI L.; FERREIRA, RENAIDE R.; DOS SANTOS, LEILA A.; GASPARIN, REBECA M.; FERNANDES, LILIAM; LANDGRAF, MARISTELLA A.; LANDGRAF, RICHARDT G.. Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide. Mediators of Inflammation, . (14/18760-4, 10/01404-0, 12/51104-8, 17/02042-3)
LOIOLA, RODRIGO A.; TORRES, TATHIANY C.; LANDGRAF, RICHARDT G.; PESQUERO, JOAO BOSCO; FERNANDES, LILIAM. Cellular Changes Induced by Kinin B-1 Receptor Deletion: Study of Endothelial Nitric Oxide Metabolism. INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS, v. 21, n. 3, p. 375-382, . (14/18760-4, 08/06676-8, 10/01404-0)
TUDELA, RENATO C.; LOIOLA, RODRIGO A.; TORRES, TATHIANY C.; GIL, NOEMI L.; ASSUNCAO, NILSON A.; DE NORONHA, SAMUEL M. R.; CORREA-NORONHA, SILVANA A.; LANDGRAF, RICHARDT G.; FERNANDES, LILIAM. L-Arginine Transport and Nitric Oxide Production in Kinin Receptor B-1(-/-) Endothelial Cells. PROTEIN AND PEPTIDE LETTERS, v. 22, n. 12, p. 1111-1116, . (10/01404-0, 14/18760-4)

Please report errors in scientific publications list using this form.