Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1
| Autor: | Lloréns, Silvia, Miranda Alonso, Francisco Javier, Alabadí Ferrer, José Antonio, González Marrachelli, Vannina Elena, Alborch Domínguez, Enrique |
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| Rok vydání: | 2004 |
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| Zdroj: | 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 RODERIC. Repositorio Institucional de la Universitat de Valéncia instname |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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