File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effect of vibration on a canine cutaneous artery

TitleEffect of vibration on a canine cutaneous artery
Authors
Issue Date1986
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, 1986, v. 250 n. 3, p. 19/3 How to Cite?
AbstractVibration of rings of isolated canine saphenous arteries depressed contractions induced by potassium chloride, prostaglandin F(2α), and activation of the adrenergic nerve endings by electrical stimulation. Peak contractions to exogenous norepinephrine were not significantly affected by vibration, being augmented, unchanged, or depressed, whereas contractions during the stable plateau phase were depressed. The calcium entry blocker diltiazem reduced the peak response but not the stable plateau phase of the contraction to norepinephrine; in the presence of diltiazem, vibration still depressed the latter. When vibration was applied during the steady state of contractions evoked by electrical stimulation, the depression was immediate, and its extent increased with both the amplitude (0.025-0.10 mm) and the frequency (30-150 Hz) of vibration. In arteries labeled with [3H]norepinephrine, vibration (120 Hz, 0.1 mm amplitude) during electrical stimulation induced a slight but significant increase in the release of labeled transmitter. It is suggested that the depression of contractions to potassium ions, prostaglandin F(2α), sympathetic nerve stimulation, and the plateau phase of the response to exogenous norepinephrine are caused by vibration depressing the force-generating process in vascular smooth muscle. Failure of vibration to significantly depress the peak contraction to norepinephrine may be explained by the facilitation by vibration of the influx of extracellular calcium ions.
Persistent Identifierhttp://hdl.handle.net/10722/170811
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLindblad, LEen_US
dc.contributor.authorLorenz, RRen_US
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:58Z-
dc.date.available2012-10-30T06:10:58Z-
dc.date.issued1986en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1986, v. 250 n. 3, p. 19/3en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/170811-
dc.description.abstractVibration of rings of isolated canine saphenous arteries depressed contractions induced by potassium chloride, prostaglandin F(2α), and activation of the adrenergic nerve endings by electrical stimulation. Peak contractions to exogenous norepinephrine were not significantly affected by vibration, being augmented, unchanged, or depressed, whereas contractions during the stable plateau phase were depressed. The calcium entry blocker diltiazem reduced the peak response but not the stable plateau phase of the contraction to norepinephrine; in the presence of diltiazem, vibration still depressed the latter. When vibration was applied during the steady state of contractions evoked by electrical stimulation, the depression was immediate, and its extent increased with both the amplitude (0.025-0.10 mm) and the frequency (30-150 Hz) of vibration. In arteries labeled with [3H]norepinephrine, vibration (120 Hz, 0.1 mm amplitude) during electrical stimulation induced a slight but significant increase in the release of labeled transmitter. It is suggested that the depression of contractions to potassium ions, prostaglandin F(2α), sympathetic nerve stimulation, and the plateau phase of the response to exogenous norepinephrine are caused by vibration depressing the force-generating process in vascular smooth muscle. Failure of vibration to significantly depress the peak contraction to norepinephrine may be explained by the facilitation by vibration of the influx of extracellular calcium ions.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.meshArteries - Physiologyen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshSkin - Blood Supplyen_US
dc.subject.meshTritium - Diagnostic Useen_US
dc.subject.meshVibrationen_US
dc.titleEffect of vibration on a canine cutaneous arteryen_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.pmid3456723-
dc.identifier.scopuseid_2-s2.0-0022479320en_US
dc.identifier.volume250en_US
dc.identifier.issue3en_US
dc.identifier.spage19/3en_US
dc.identifier.isiWOS:A1986A526900024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLindblad, LE=19735934700en_US
dc.identifier.scopusauthoridLorenz, RR=7402095192en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats