Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent
| dc.date.accessioned | 2011-02-10T15:18:28Z | |
| dc.date.available | 2011-02-10T15:18:28Z | |
| dc.identifier.citation | SILVEIRA, E. A. et al. Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent. Braz J Med Biol Res, Ribeirão Preto, v. 43, n. 5, p. 492-499, maio 2010. Disponível em: <http://www.scielo.br/pdf/bjmbr/v43n5/82.pdf>. Acesso em: 7 fev. 2011. | por |
| dc.identifier.doi | 10.1590/S0100-879X2010007500027 | |
| dc.identifier.issn | 0100-879X | |
| dc.identifier.uri | http://repositorio.ufes.br/handle/10/587 | |
| dc.rights | open access | en |
| dc.title | Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent | por |
| dc.type | article | en |
| dcterms.abstract | Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentration-response curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E+), lead acetate increased maximal response (Emax) (control: 364.4 ± 36, Pb2+: 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD2; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E-) lead had no effect but increased baseline perfusion pressure (E+: 79.5 ± 2.4, E-: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on Emax and pD2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenase-derived vasoconstrictors and involving reactive oxygen species. | eng |
| dcterms.creator | Silveira, Eduardo Almeida da | |
| dcterms.creator | Lizardo, Juliana Hott de Fúcio | |
| dcterms.creator | Souza, L.P. | |
| dcterms.creator | Stefanon, Ivanita | |
| dcterms.creator | Vassallo, Dalton Valentim | |
| dcterms.issued | 2010-05 | |
| dcterms.language | eng | en |
| dcterms.subject | Endotélio | por |
| dcterms.subject | Hipertensão | por |
| dcterms.subject | Lead acetate | eng |
| dcterms.subject | Vascular reactivity | eng |
| dcterms.subject | Endothelium | eng |
| dcterms.subject | Hypertension | eng |