Endothelin Et(a) Receptor Antagonism Attenuates The Pressor Effects Of Nicotine In Rats.

dc.creatorTanus-Santos, J E
dc.creatorSampaio, R C
dc.creatorHyslop, S
dc.creatorFranchini, K G
dc.creatorMoreno, H
dc.date2000-May
dc.date2015-11-27T12:22:59Z
dc.date2015-11-27T12:22:59Z
dc.date.accessioned2018-03-29T00:55:00Z
dc.date.available2018-03-29T00:55:00Z
dc.identifierEuropean Journal Of Pharmacology. v. 396, n. 1, p. 33-7, 2000-May.
dc.identifier0014-2999
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/10822051
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194752
dc.identifier10822051
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1294985
dc.descriptionThe increased endothelin-1 levels observed after smoking may result from nicotine-stimulated endothelin-1 production by endothelial cells. In this study, we investigated the effects of selective endothelin ET(A) receptors antagonist Cycle D-a-aspartyl-L-prolyl-D-isoleucyl-D-tryptophyl (JKC 301) and of endothelin ET(B) receptors antagonist N-cis-2, 6-dimethylpiperidino-carbonyl-L-gamma-methyl-leucyl-D-L-m ethoxycarbonyl-tryptophanyl-norleucine (BQ 788) on the changes in mean arterial pressure, heart rate, and plasma thromboxane B(2) (the stable product of thromboxane A(2)) levels caused by increasing doses of nicotine (0.6, 2, 6, and 20 micromol/kg) in anesthetised rats. Nicotine (0.6, 2, and 6 micromol/kg) significantly increased the mean arterial pressure in control and BQ 788-pretreated rats, while only a nicotine dose of 2 micromol/kg) increased the mean arterial pressure in JKC 301-pretreated animals. There were no differences in the nicotine-induced changes in heart rate or in the increases in thromboxane B(2) levels among the groups treated with saline, JKC 301 and BQ 788. These results demonstrate that whereas the antagonism of endothelin ET(A) receptors attenuated the increase in blood pressure after nicotine injections, endothelin ET(B) receptor antagonism had no such effect. In addition, the antagonism of endothelin ET(A) or ET(B) receptors did not affect thromboxane A(2) production after nicotine administration. These findings suggest that endothelin-1 may have a role in the acute effects of nicotine.
dc.description396
dc.description33-7
dc.languageeng
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectBlood Pressure
dc.subjectEndothelin Receptor Antagonists
dc.subjectHeart Rate
dc.subjectMale
dc.subjectNicotine
dc.subjectNicotinic Agonists
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReceptor, Endothelin A
dc.subjectReceptor, Endothelin B
dc.subjectThromboxane B2
dc.titleEndothelin Et(a) Receptor Antagonism Attenuates The Pressor Effects Of Nicotine In Rats.
dc.typeArtículos de revistas


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