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Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

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Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

dc.contributor.author	Lloréns, Silvia
dc.contributor.author	Miranda Alonso, Francisco Javier
dc.contributor.author	Alabadí Ferrer, José Antonio
dc.contributor.author	González Marrachelli, Vannina Elena
dc.contributor.author	Alborch Domínguez, Enrique
dc.date.accessioned	2014-02-11T13:51:35Z
dc.date.available	2014-02-11T13:51:35Z
dc.date.issued	2004
dc.identifier.citation	Lloréns, Silvia Miranda Alonso, Francisco Javier Alabadí Ferrer, José Antonio González Marrachelli, Vannina Elena Alborch Dominguez, Enrique 2004 Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1. European Journal of Pharmacology 486 43 51
dc.identifier.uri	http://hdl.handle.net/10550/32881
dc.description.abstract	The influence of diabetes on regulatory mechanisms and specific receptors implicated in the contractile response of isolated rabbit carotid arteries to endothelin-1 was examined. Endothelin-1 induced a concentration-dependent contraction that was greater in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal or NG-nitro-L-arginine enhanced contractions in response to endothelin-1 only in control arteries, without modifying the endothelin-1 response in diabetic arteries. Indomethacin, furegrelate (thromboxane A2 inhibitor), or cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123; endothelin ETA receptor antagonist) inhibited the contractions in response to endothelin-1, the inhibition being greater in diabetic arteries than in control arteries. 2,6-Dimethylpiperidinecarbonyl-g-methyl-Leu-Nin- (methoxycarbonyl)-D-Trp-D-Nle (BQ-788; endothelin ETB receptor antagonist) enhanced the contraction elicited by endothelin-1 in control arteries and displaced to the right the contractile curve for endothelin-1 in diabetic arteries. In summary, diabetes induces hyperreactivity of the rabbit carotid artery to endothelin-1 by a mechanism that at least includes: (1) enhanced activity of muscular endothelin ETA receptors; (2) impairment of endothelin ETB receptor-mediated nitric oxide (NO) release; and (3) enhancement of the production of thromboxane A2.
dc.relation.ispartof	European Journal of Pharmacology, 2004, vol. 486, p. 43-51
dc.subject	Endoteli vascular
dc.subject	Diabetis
dc.subject	Òxid nítric
dc.subject	Artèries
dc.title	Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1
dc.type	journal article	es_ES
dc.date.updated	2014-02-11T13:51:35Z
dc.identifier.idgrec	014188
dc.rights.accessRights	open access	es_ES