dc.contributorFaculdades Unificadas da Fundação Educacional de Barretos
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:22:43Z
dc.date.accessioned2022-10-05T18:10:15Z
dc.date.available2014-05-27T11:22:43Z
dc.date.available2022-10-05T18:10:15Z
dc.date.created2014-05-27T11:22:43Z
dc.date.issued2007-12-01
dc.identifierRevista de Ciencias Farmaceuticas Basica e Aplicada, v. 28, n. 3, p. 341-345, 2007.
dc.identifier1808-4532
dc.identifierhttp://hdl.handle.net/11449/70134
dc.identifier2-s2.0-50049092037
dc.identifier2-s2.0-50049092037.pdf
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3919477
dc.description.abstractSeptic shock or sepsis is reported to be one of the major causes of death when followed by systemic infectious trauma in humans and other mammals. Its development leads to a large drop in blood pressure and a reduction in vascular responsiveness to physiological vasoconstrictors which, if not contained, can lead to death. It is proposed that this vascular response is due to the action of bacterial cell wall products released into the bloodstream by the vascular endothelium and is considered a normal response of the body's defenses against infection. A reduction in vascular reactivity to epinephrine and norepinephrine is observed under these conditions. In the present study in rats, the aim was to assess whether those effects of hypotension and hyporeactivity are also related to another endogenous vasoconstrictor, angiotensin II (AII). We evaluated the variation in the power of this vasoconstrictor over the mean arterial pressure in anesthetized rats, before and after the establishment of hypotension by Escherichia coli endotoxin (Etx). Our results show that in this model of septic shock, there is a reduction in vascular reactivity to AII and this reduction can be reversed by the inhibitor of nitric oxide synthase, Nω-Nitro-L- Arginine (NωNLA). Our results also suggest that other endogenous factors (not yet fully known) are involved in the protection of rats against septic shock, in addition to the L-arginine NO pathway.
dc.languageeng
dc.relationRevista de Ciências Farmacêuticas Básica e Aplicada
dc.relation0,131
dc.rightsAcesso aberto
dc.sourceScopus
dc.subjectAngiotensin II
dc.subjectNωNLA Escherichia coli endotoxin
dc.subjectNO
dc.subjectRat
dc.subjectVascular hyporeactivity
dc.subjectadrenalin
dc.subjectangiotensin II
dc.subjectarginine
dc.subjectEscherichia coli endotoxin
dc.subjectn(g) nitroarginine
dc.subjectnitric oxide
dc.subjectnitric oxide synthase
dc.subjectnoradrenalin
dc.subjectvasoconstrictor agent
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectbacterial cell wall
dc.subjectblood vessel reactivity
dc.subjectcontrolled study
dc.subjectdisease model
dc.subjectenzyme inhibition
dc.subjecthypotension
dc.subjectinfection
dc.subjectmale
dc.subjectmean arterial pressure
dc.subjectnonhuman
dc.subjectprotection
dc.subjectrat
dc.subjectsepsis
dc.subjectseptic shock
dc.subjectWistar rat
dc.titleVascular hyporeactivity to angiotensin II induced by Escherichia coli endotoxin is reversed by Nω-Nitro-L-Arginine, an inhibitor of nitric oxide synthase
dc.typeArtigo


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