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Article: Reduced production of cGMP underlies the loss of endothelium-dependent relaxations in the canine basilar artery after subarachnoid hemorrhage

TitleReduced production of cGMP underlies the loss of endothelium-dependent relaxations in the canine basilar artery after subarachnoid hemorrhage
Authors
Issue Date1992
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1992, v. 70 n. 2, p. 248-256 How to Cite?
AbstractEndothelium-dependent relaxations are inhibited during chronic vasospasm after subarachnoid hemorrhage in the canine basilar artery, although the luminal release of endothelium-derived relaxing factor (EDRF) is maintained. The present study investigated the mechanisms underlying the impaired vascular reactivity and in particular whether the loss of responsiveness of the smooth muscle to EDRF is due to an impaired production of cGMP. Bradykinin and nitric oxide evoked concentration-dependent relaxations in isolated canine basilar arteries with and without endothelium, respectively, which were reduced in the subarachnoid hemorrhage group. Relaxations evoked by M and B22,948 (an inhibitor of cGMP phosphodiesterases) were smaller, but those evoked by the lipophilic cGMP analogue 8-bromo-cGMP were potentiated slightly in the subarachnoid hemorrhage group. The resting levels of cGMP in rings with endothelium (reflecting the effect of spontaneous release of EDRF) and those evoked by bradykinin in rings with endothelium and by nitric oxide in rings without endothelium were diminished in the subarachnoid hemorrhage group. These data indicate that the altered endothelium-mediated relaxations of the smooth muscle after subarachnoid hemorrhage is due, at least in part, to an impaired activation of soluble guanylate cyclase leading to a reduced production of cGMP in the smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/171055
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKim, Pen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorSundt Jr, TMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:00Z-
dc.date.available2012-10-30T06:12:00Z-
dc.date.issued1992en_US
dc.identifier.citationCirculation Research, 1992, v. 70 n. 2, p. 248-256en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/171055-
dc.description.abstractEndothelium-dependent relaxations are inhibited during chronic vasospasm after subarachnoid hemorrhage in the canine basilar artery, although the luminal release of endothelium-derived relaxing factor (EDRF) is maintained. The present study investigated the mechanisms underlying the impaired vascular reactivity and in particular whether the loss of responsiveness of the smooth muscle to EDRF is due to an impaired production of cGMP. Bradykinin and nitric oxide evoked concentration-dependent relaxations in isolated canine basilar arteries with and without endothelium, respectively, which were reduced in the subarachnoid hemorrhage group. Relaxations evoked by M and B22,948 (an inhibitor of cGMP phosphodiesterases) were smaller, but those evoked by the lipophilic cGMP analogue 8-bromo-cGMP were potentiated slightly in the subarachnoid hemorrhage group. The resting levels of cGMP in rings with endothelium (reflecting the effect of spontaneous release of EDRF) and those evoked by bradykinin in rings with endothelium and by nitric oxide in rings without endothelium were diminished in the subarachnoid hemorrhage group. These data indicate that the altered endothelium-mediated relaxations of the smooth muscle after subarachnoid hemorrhage is due, at least in part, to an impaired activation of soluble guanylate cyclase leading to a reduced production of cGMP in the smooth muscle.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.mesh3',5'-Cyclic-Gmp Phosphodiesterases - Antagonists & Inhibitorsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBasilar Artery - Metabolism - Physiopathologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCyclic Gmp - Biosynthesisen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Metabolism - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshPurinones - Pharmacologyen_US
dc.subject.meshRadioimmunoassayen_US
dc.subject.meshSubarachnoid Hemorrhage - Metabolism - Physiopathologyen_US
dc.subject.meshVasodilationen_US
dc.titleReduced production of cGMP underlies the loss of endothelium-dependent relaxations in the canine basilar artery after subarachnoid hemorrhageen_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.pmid1310445-
dc.identifier.scopuseid_2-s2.0-0026586194en_US
dc.identifier.volume70en_US
dc.identifier.issue2en_US
dc.identifier.spage248en_US
dc.identifier.epage256en_US
dc.identifier.isiWOS:A1992HC55400005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKim, P=7402334666en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridSundt Jr, TM=34572694400en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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