dc.creatorFaro, R
dc.creatorGrassi-Kassisse, D M
dc.creatorDonato, J L
dc.creatorBoin, I
dc.creatorOpgenorth, T J
dc.creatorWithrington, P G
dc.creatorZatz, R
dc.creatorAntunes, E
dc.creatorde Nucci, G
dc.date1995
dc.date2015-11-27T12:18:38Z
dc.date2015-11-27T12:18:38Z
dc.date.accessioned2018-03-29T00:51:36Z
dc.date.available2018-03-29T00:51:36Z
dc.identifierJournal Of Cardiovascular Pharmacology. v. 26 Suppl 3, p. S204-7, 1995.
dc.identifier0160-2446
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/8587363
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/193866
dc.identifier8587363
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294099
dc.descriptionThe vascular effects of endothelin-1 (ET-1; ETA/ETB agonist), sarafotoxin 6b (S6b; ETA agonist), and IRL 1620 (ETB agonist) were investigated in the isolated canine liver arterial circuit before and after infusions of indomethacin (cyclo-oxygenase inhibitor) and N omega L-nitro arginine methyl ester (L-NAME; nitric oxide synthesis inhibitor). Norepinephrine (NE) was used as vasconstrictor control agent. The portal vein, hepatic artery, and vena cava were cannulated in vitro and the liver was perfused via the hepatic artery and portal vein with oxygenated (95%) O2/5% CO2) Krebs solution at 37 degrees C. Intra-arterial bolus injections of either ET-1 (0.4-400 pmol) or S6b (0.4-400 pmol) induced dose-dependent and long-lasting vasoconstriction accompanied by significant prostacyclin release. The vasoconstrictor responses to these peptides were slightly increased during infusion of indomethacin. Subsequent infusion of L-NAME potentiated both ET-1- and S6b-induced vasoconstriction (p < 0.05). IRL 1620 (up to 1.2 nmol) had no effect on the hepatic arterial vascular resistance even during indomethacin and L-NAME infusions. Infusion of the ETA receptor antagonist FR-139317 (0.3 microM) markedly reduced both ET-1- and S6b-induced vasoconstriction without affecting that evoked by NE. Our results indicate that pressor responses to ET-1 and S6b in the isolated canine liver are modulated by concomitant release of vasodilator mediators, including prostacyclin and nitric oxide. These effects appear to depend primarily on the activation of ETA receptor subtypes. IRL 1620 (but not ET-1) induced a significant release of hemoglobin into the venous effluent, suggesting that ETB receptors are located in the venous side of the intrahepatic circulation.
dc.description26 Suppl 3
dc.descriptionS204-7
dc.languageeng
dc.relationJournal Of Cardiovascular Pharmacology
dc.relationJ. Cardiovasc. Pharmacol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectArginine
dc.subjectAzepines
dc.subjectDogs
dc.subjectEndothelins
dc.subjectFemale
dc.subjectHemoglobins
dc.subjectHepatic Artery
dc.subjectIn Vitro Techniques
dc.subjectIndoles
dc.subjectIndomethacin
dc.subjectMale
dc.subjectNg-nitroarginine Methyl Ester
dc.subjectPeptide Fragments
dc.subjectReceptor, Endothelin A
dc.subjectReceptor, Endothelin B
dc.subjectReceptors, Endothelin
dc.subjectViper Venoms
dc.titleRole Of Endothelin Eta And Etb Receptors In The Arterial Vasculature Of The Isolated Canine Liver.
dc.typeArtículos de revistas


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