Diabetes-induced changes in endothelial mechanisms implicated in rabbit carotid arterial response to 5-hydroxytryptamine

被引：18

作者：

Miranda, FJ

Alabadí, JA

Lloréns, S

de Apodaca, RFR

Centeno, JM

Alborch, E

机构：

[1] Univ Valencia, Fac Farm, Dept Fisiol, Valencia 46100, Spain

[2] Hosp La Fe, Res Ctr, E-46009 Valencia, Spain

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2000年 / 401卷 / 03期

关键词：

endothelium; diabetes; nitric oxide (NO); 5-HT; (5-hydroxytryptamine; serotonin); carotid artery;

D O I：

10.1016/S0014-2999(00)00469-6

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The influence of diabetes on endothelial mechanisms implicated in the response of isolated rabbit carotid arteries to 5-hydroxytryptamine (5-HT) was studied. 5-HT induced a concentration-dependent contraction that was potentiated in arteries from diabetic rabbits with respect to that in arteries from control rabbits. Endothelium removal potentiated 5-HT contractions in arteries from both control and diabetic rabbits but increased the maximum effect only in arteries from diabetic rabbits. Incubation of arterial segments with N-G-nitro-L-arginine (L-NA) enhanced the contractile response to 5-HT. This L-NA enhancement was greater in arteries from diabetic rabbits than in arteries from control rabbits. Aminoguanidine did not modify the 5-HT contraction in arteries from control and diabetic rabbits. Indomethacin inhibited the 5-HT-induced response, and this inhibition was higher in arteries from control rabbits than in arteries from diabetic rabbits. In summary, diabetes enhances the sensitivity of the rabbit carotid artery to 5-HT. In control animals, the endothelium modulated the arterial response to 5-HT by the release of both nitric oxide (NO) and a vasoconstrictor prostanoid. Diabetes enhances endothelial constitutive NO activity and impairs the production of the endothelial vasoconstrictor. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

页码：397 / 402

页数：6

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