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dc.contributor.author | Alabadí Ferrer, José Antonio | |
dc.contributor.author | Miranda Alonso, Francisco Javier | |
dc.contributor.author | Lloréns, Silvia | |
dc.contributor.author | Centeno Guil, José M. | |
dc.contributor.author | González Marrachelli, Vannina Elena | |
dc.contributor.author | Alborch Domínguez, Enrique | |
dc.date.accessioned | 2013-12-09T13:51:47Z | |
dc.date.available | 2013-12-09T13:51:47Z | |
dc.date.issued | 2004 | |
dc.identifier.citation | Alabadí Ferrer, José Antonio Miranda Alonso, Francisco Javier Lloréns, Silvia Centeno Guil, José M González Marrachelli, Vannina Elena Alborch Dominguez, Enrique 2004 Mechanisms underlying diabetes enhancement of endothelin-1-induced contraction in rabbit basilar artery. European Journal of Pharmacology 486 289 296 | |
dc.identifier.uri | http://hdl.handle.net/10550/32082 | |
dc.description.abstract | The influence of alloxan-induced diabetes on the reactivity of rabbit basilar artery to endothelin-1 was examined. Endothelin-1 induced concentration-dependent contraction of basilar arteries that was higher in diabetic than in control rabbits. Endothelium removal produced a higher enhancement of the endothelin-1-induced contraction in control than in diabetic rabbits. NG-nitro-L-arginine (L-NOArg) enhanced the maximal contraction induced by endothelin-1 in control rabbits and potentiated this response in diabetic rabbits. Endothelin ETA receptor antagonist, cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123), inhibited endothelin-1-induced contraction in both rabbit groups. Endothelin ETB receptor antagonist, 2,6-Dimethylpiperidinecarbonyl-g-Methyl Leu-Nin-(Methoxycarbonyl)-D-Trp-D-Nle (BQ-788), enhanced endothelin-1-induced contraction in control rabbits and decreased the potency of endothelin-1 in diabetic rabbits. Sodium nitroprusside-induced relaxation of basilar arteries was lower in diabetic than in control rabbits. These results suggest that mechanisms underlying rabbit basilar artery hyperreactivity to endothelin-1 include decreased endothelial modulation of endothelin-1-induced contraction, with impaired endothelial endothelin ETB receptor activity; decreased sensitivity to nitric oxide (NO) in vascular smooth muscle; and enhanced participation of muscular endothelin ETA and ETB receptors. | |
dc.relation.ispartof | European Journal of Pharmacology, 2004, vol. 486, p. 289-296 | |
dc.subject | Endoteli vascular | |
dc.subject | Òxid nítric | |
dc.subject | Diabetis | |
dc.subject | Artèries | |
dc.title | Mechanisms underlying diabetes enhancement of endothelin-1-induced contraction in rabbit basilar artery | |
dc.type | journal article | es_ES |
dc.date.updated | 2013-12-09T13:51:47Z | |
dc.identifier.doi | 10.1016/j.ejphar.2004.01.005 | |
dc.identifier.idgrec | 014187 | |
dc.rights.accessRights | open access | es_ES |
dc.identifier.url | 10.1016/j.ejphar.2004.01.005 |