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Article: Increased spontaneous tone in renal arteries of spontaneously hypertensive rats

TitleIncreased spontaneous tone in renal arteries of spontaneously hypertensive rats
Authors
Issue Date2007
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, 2007, v. 293 n. 3, p. H1673-H1681 How to Cite?
AbstractThe spontaneous tone of vascular smooth muscle is augmented in hypertension. The present study examined the role of nitric oxide (NO), cyclooxygenase (COX), thromboxane A2/prostanoid (TP) and PGE 2/prostanoid (EP-1) receptors, reactive oxygen species, and large-conductance Ca2+-activated K+ (BKCa) channels in the regulation of spontaneous tone in renal arteries of young and mature Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Rings of arteries, with and without endothelium, were suspended in a myograph for isometric force recording. Spontaneous tone (increase above initial tension) was observed only in arteries of mature SHR and was greater in arteries without endothelium. Nω-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthases) induced larger contractions in arteries of SHR than WKY. Indomethacin (a COX inhibitor), SC-19220 (an EP-1 receptor antagonist), and terutroban (a TP receptor antagonist) reduced the L-NAME-evoked contractions. Tiron (a superoxide anion scavenger), catalase (an enzyme that degrades H 2O2), and deferoxamine (a hydroxyl radical scavenger) augmented the L-NAME-induced contractions in arteries of mature SHR. Charybdotoxin (a BKCa channel blocker) caused contractions in arteries of mature SHR without endothelium and in arteries with endothelium incubated with L-NAME. A decreased protein level of endothelial NO synthase, an increased release of prostacyclin, and an increased expression of EP-1 receptors were observed in arteries of mature SHR. The present study suggests that spontaneous tone is precipitated by age and hypertension. The reduced production of NO, leading to decreased activation of BKCa channels, may leave the actions of endogenous vasoconstrictors unopposed. COX products that activate EP-1 and TP receptors are involved in the development of spontaneous tone. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/171358
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMichel, FSen_US
dc.contributor.authorMan, RYKen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:35Z-
dc.date.available2012-10-30T06:13:35Z-
dc.date.issued2007en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2007, v. 293 n. 3, p. H1673-H1681en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171358-
dc.description.abstractThe spontaneous tone of vascular smooth muscle is augmented in hypertension. The present study examined the role of nitric oxide (NO), cyclooxygenase (COX), thromboxane A2/prostanoid (TP) and PGE 2/prostanoid (EP-1) receptors, reactive oxygen species, and large-conductance Ca2+-activated K+ (BKCa) channels in the regulation of spontaneous tone in renal arteries of young and mature Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Rings of arteries, with and without endothelium, were suspended in a myograph for isometric force recording. Spontaneous tone (increase above initial tension) was observed only in arteries of mature SHR and was greater in arteries without endothelium. Nω-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthases) induced larger contractions in arteries of SHR than WKY. Indomethacin (a COX inhibitor), SC-19220 (an EP-1 receptor antagonist), and terutroban (a TP receptor antagonist) reduced the L-NAME-evoked contractions. Tiron (a superoxide anion scavenger), catalase (an enzyme that degrades H 2O2), and deferoxamine (a hydroxyl radical scavenger) augmented the L-NAME-induced contractions in arteries of mature SHR. Charybdotoxin (a BKCa channel blocker) caused contractions in arteries of mature SHR without endothelium and in arteries with endothelium incubated with L-NAME. A decreased protein level of endothelial NO synthase, an increased release of prostacyclin, and an increased expression of EP-1 receptors were observed in arteries of mature SHR. The present study suggests that spontaneous tone is precipitated by age and hypertension. The reduced production of NO, leading to decreased activation of BKCa channels, may leave the actions of endogenous vasoconstrictors unopposed. COX products that activate EP-1 and TP receptors are involved in the development of spontaneous tone. Copyright © 2007 the American Physiological Society.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.meshDisease Models, Animalen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Hypertonia - Physiopathologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPotassium Channels - Physiologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Physiologyen_US
dc.subject.meshProstaglandins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshReceptors, Prostaglandin E - Physiologyen_US
dc.subject.meshReceptors, Prostaglandin E, Ep1 Subtypeen_US
dc.subject.meshReceptors, Thromboxane A2, Prostaglandin H2 - Physiologyen_US
dc.subject.meshRenal Artery - Physiopathologyen_US
dc.titleIncreased spontaneous tone in renal arteries of spontaneously hypertensive ratsen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajpheart.00289.2007en_US
dc.identifier.pmid17557920-
dc.identifier.scopuseid_2-s2.0-34548396787en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548396787&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume293en_US
dc.identifier.issue3en_US
dc.identifier.spageH1673en_US
dc.identifier.epageH1681en_US
dc.identifier.isiWOS:000249237800045-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMichel, FS=7402556401en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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