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RESEARCH PRODUCT
Diabetes-induced changes in endothelial mechanisms implicated in rabbit carotid arterial response to 5-hydroxytryptamine
Francisco J. MirandaJosé A. AlabadíEnrique AlborchRosa F Ruiz De ApodacaSilvia LlorensJosé M. Centenosubject
MaleSerotoninmedicine.medical_specialtyContraction (grammar)ArginineEndotheliumIndomethacinIn Vitro TechniquesGuanidinesNitroarginineDiabetes Mellitus ExperimentalNitric oxidechemistry.chemical_compoundInternal medicineDiabetes mellitusmedicineAnimalsEnzyme InhibitorsPharmacologyLagomorphaDose-Response Relationship DrugbiologyVascular diseasebusiness.industryProstanoidmedicine.diseasebiology.organism_classificationCarotid Arteriesmedicine.anatomical_structureEndocrinologychemistryVasoconstrictionKetamineEndothelium VascularRabbitsNitric Oxide Synthasebusinessdescription
Abstract 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.
year | journal | country | edition | language |
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2000-08-01 | European Journal of Pharmacology |