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Article: The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - Induced diabetic rats is restored by 5-methyltetrahydrofolate

TitleThe impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - Induced diabetic rats is restored by 5-methyltetrahydrofolate
Authors
Issue Date2000
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00125/index.htm
Citation
Diabetologia, 2000, v. 43 n. 9, p. 1116-1125 How to Cite?
AbstractAims/hypothesis. Endothelial dysfunction contributes to the development of diabetic vascular complications. A better understanding of the pathophysiology of endothelial dysfunction in diabetes could lead to new approaches to prevent microvascular disease. Methods. Endothelium-dependent and endothelium-independent vasodilator responses were investigated in the renal microcirculation of streptozotocin-induced diabetic rats. We measured renal blood flow changes with an electromagnetic flow probe. In addition, the responses of the different segments of the renal microcirculation were evaluated with videomicroscopy using the hydronephrotic kidney technique. Because endothelial cells release different relaxing factors (nitric oxide, prostacyclin and an unidentified endothelium-derived hyperpolarizing factor), responses to acetylcholine were measured before and after treatment with the nitric oxide synthase inhibitor L-N(G)-nitroarginine methylester HCI (L-NAME) and the cyclooxygenase inhibitor indomethacin. We evaluated with the effect of 5-methyltetrahydrofolate, the active form of folate, on the responses. Results. The L-NAME- and indomethacin-resistant vasodilation to intra-renal acetylcholine was significantly reduced in the diabetic compared with control rats, suggesting impaired endothelium-derived hyperpolarizing factor-mediated vasodilation. The responses to the nitric oxide donor (Z)-1-[-2-(aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) and to the K+-channel opener pinacidil were similar in diabetics and controls, indicating intact endothelium-independent vasodilator mechanisms. The contribution of endothelium-derived hyperpolarizing factor to vasodilation induced by acetylcholine was greatest in the smallest arterioles. In diabetic rats, the response to acetylcholine was increasingly impared as vessel size decreased. Defective vasodilation in diabetic kidneys was rapidly normalized by 5-methyltetrahydrofolate. Conclusion-interpretation. Endothelium-derived hyperpolarizing factor-mediated vasodilation is impaired in the renal microcirculation of diabetic rats, in particular in the smallest arteries. Treatment with folate restores the impaired endothelial function in diabetes.
Persistent Identifierhttp://hdl.handle.net/10722/171234
ISSN
2015 Impact Factor: 6.206
2015 SCImago Journal Rankings: 3.528
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDe Vriese, ASen_US
dc.contributor.authorVan De Voorde, Jen_US
dc.contributor.authorBlom, HJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorVerbeke, Men_US
dc.contributor.authorLameire, NHen_US
dc.date.accessioned2012-10-30T06:12:51Z-
dc.date.available2012-10-30T06:12:51Z-
dc.date.issued2000en_US
dc.identifier.citationDiabetologia, 2000, v. 43 n. 9, p. 1116-1125en_US
dc.identifier.issn0012-186Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171234-
dc.description.abstractAims/hypothesis. Endothelial dysfunction contributes to the development of diabetic vascular complications. A better understanding of the pathophysiology of endothelial dysfunction in diabetes could lead to new approaches to prevent microvascular disease. Methods. Endothelium-dependent and endothelium-independent vasodilator responses were investigated in the renal microcirculation of streptozotocin-induced diabetic rats. We measured renal blood flow changes with an electromagnetic flow probe. In addition, the responses of the different segments of the renal microcirculation were evaluated with videomicroscopy using the hydronephrotic kidney technique. Because endothelial cells release different relaxing factors (nitric oxide, prostacyclin and an unidentified endothelium-derived hyperpolarizing factor), responses to acetylcholine were measured before and after treatment with the nitric oxide synthase inhibitor L-N(G)-nitroarginine methylester HCI (L-NAME) and the cyclooxygenase inhibitor indomethacin. We evaluated with the effect of 5-methyltetrahydrofolate, the active form of folate, on the responses. Results. The L-NAME- and indomethacin-resistant vasodilation to intra-renal acetylcholine was significantly reduced in the diabetic compared with control rats, suggesting impaired endothelium-derived hyperpolarizing factor-mediated vasodilation. The responses to the nitric oxide donor (Z)-1-[-2-(aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) and to the K+-channel opener pinacidil were similar in diabetics and controls, indicating intact endothelium-independent vasodilator mechanisms. The contribution of endothelium-derived hyperpolarizing factor to vasodilation induced by acetylcholine was greatest in the smallest arterioles. In diabetic rats, the response to acetylcholine was increasingly impared as vessel size decreased. Defective vasodilation in diabetic kidneys was rapidly normalized by 5-methyltetrahydrofolate. Conclusion-interpretation. Endothelium-derived hyperpolarizing factor-mediated vasodilation is impaired in the renal microcirculation of diabetic rats, in particular in the smallest arteries. Treatment with folate restores the impaired endothelial function in diabetes.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00125/index.htmen_US
dc.relation.ispartofDiabetologiaen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshBiological Markers - Blooden_US
dc.subject.meshBlood Pressureen_US
dc.subject.meshDiabetes Mellitus, Experimental - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFructosamine - Blooden_US
dc.subject.meshHydronephrosis - Physiopathologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshKidney - Blood Supplyen_US
dc.subject.meshMicrocirculation - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshMicroscopy, Videoen_US
dc.subject.meshNg-Nitroarginine Methyl Ester - Pharmacologyen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshNitroso Compounds - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshRegional Blood Flow - Drug Effectsen_US
dc.subject.meshRenal Artery - Drug Effects - Physiopathologyen_US
dc.subject.meshRenal Circulation - Drug Effects - Physiologyen_US
dc.subject.meshTetrahydrofolates - Pharmacologyen_US
dc.subject.meshVasodilation - Drug Effects - Physiologyen_US
dc.titleThe impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - Induced diabetic rats is restored by 5-methyltetrahydrofolateen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s001250051502en_US
dc.identifier.pmid11043857-
dc.identifier.scopuseid_2-s2.0-0033816515en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033816515&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume43en_US
dc.identifier.issue9en_US
dc.identifier.spage1116en_US
dc.identifier.epage1125en_US
dc.identifier.isiWOS:000089331000005-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridDe Vriese, AS=7006417891en_US
dc.identifier.scopusauthoridVan De Voorde, J=7005936690en_US
dc.identifier.scopusauthoridBlom, HJ=7101946367en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridVerbeke, M=6701745535en_US
dc.identifier.scopusauthoridLameire, NH=35375565900en_US

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