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Article: cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries

TitlecGMP mediates the desensitization to bradykinin in isolated canine coronary arteries
Authors
Issue Date1995
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1995, v. 268 n. 2 37-2, p. H865-H870 How to Cite?
AbstractThe relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10-8 M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F(2α), and concentration- relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the elevation in guanosine 3',5'-cyclic monophosphate (cGMP) levels evoked by bradykinin was similar in both groups of tissues. The curves to bradykinin obtained in the presence of N(G)-nitro-L-arginine (an NO synthase inhibitor) were depressed, whereas those obtained in arteries contracted with potassium (to eliminate the EDHF-mediated relaxation) were not affected by the desensitization. Addition of N(G)-nitro-L-arginine, oxyhemoglobin, or methylene blue before the desensitization procedure preserved, whereas 3- morpholinosydnonimine (SIN-1, a donor of NO) and 8-bromoguanosine 3',5'- cyclic monophosphate impaired, the EDHF-mediated relaxation to bradykinin. Thus the selective impairment of the EDHF-dependent relaxation to bradykinin may be mediated by NO, acting mainly through increased production of cGMP.
Persistent Identifierhttp://hdl.handle.net/10722/171157
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorOlmos, Len_US
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorIlliano, Sen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:26Z-
dc.date.available2012-10-30T06:12:26Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1995, v. 268 n. 2 37-2, p. H865-H870en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171157-
dc.description.abstractThe relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10-8 M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F(2α), and concentration- relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the elevation in guanosine 3',5'-cyclic monophosphate (cGMP) levels evoked by bradykinin was similar in both groups of tissues. The curves to bradykinin obtained in the presence of N(G)-nitro-L-arginine (an NO synthase inhibitor) were depressed, whereas those obtained in arteries contracted with potassium (to eliminate the EDHF-mediated relaxation) were not affected by the desensitization. Addition of N(G)-nitro-L-arginine, oxyhemoglobin, or methylene blue before the desensitization procedure preserved, whereas 3- morpholinosydnonimine (SIN-1, a donor of NO) and 8-bromoguanosine 3',5'- cyclic monophosphate impaired, the EDHF-mediated relaxation to bradykinin. Thus the selective impairment of the EDHF-dependent relaxation to bradykinin may be mediated by NO, acting mainly through increased production of cGMP.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshArteries - Drug Effectsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshCyclic Gmp - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDrug Resistanceen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNitroarginineen_US
dc.subject.meshOxyhemoglobins - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshVasodilationen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titlecGMP mediates the desensitization to bradykinin in isolated canine coronary arteriesen_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.pmid7864213-
dc.identifier.scopuseid_2-s2.0-0028925129en_US
dc.identifier.volume268en_US
dc.identifier.issue2 37-2en_US
dc.identifier.spageH865en_US
dc.identifier.epageH870en_US
dc.identifier.isiWOS:A1995QF81400044-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridOlmos, L=7005286818en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridIlliano, S=6602119848en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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