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Article: Antagonist drugs and bone vascular smooth muscle

TitleAntagonist drugs and bone vascular smooth muscle
Authors
Issue Date1992
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.elsevier.com/locate/orthres
Citation
Journal Of Orthopaedic Research, 1992, v. 10 n. 1, p. 104-111 How to Cite?
AbstractAn ex vivo canine tibia model was used to quantitate the specific adrenergic subtype contribution in bone vasculature. Tibiae were obtained from mongrel dogs, the nutrient artery was catheterized, and the bone was placed in an ex vivo perfusion apparatus at constant flow. Perfusion was accomplished using oxygenated Krebs-Ringer solution. A norepinephrine dose-response curve was obtained by using incremental single bolus doses. Each bone was perfused with a vasoactive drug at a standard physiologic dosage. After 30 min of perfusion, a second norepinephrine dose-response curve was generated. The degree of attenuation of the norepinephrine dose-response curve, as determined by the total area under the curve, was interpreted as the relaxation effect of the drug on the smooth muscle of the vascular bed. Prazosin (α1-receptor antagonist), rauwolszin (α2-receptor antagonist), propranolol (β-receptor antagonist), and diltiazem (calcium-entry inhibitor) were evaluated. Our data suggest that α1 and α2 adrenergic receptor antagonism results in a quantitatively similar attenuation of norepinephrine-induced vascular smooth muscle contraction. Calcium-entry antagonism produced less, but significant, attenuation of smooth muscle contractility. Beta-adrenergic receptor blockade yielded only a slight, although consistent, reduction in reactivity. | An ex vivo canine tibia model was used to quantitate the specific adrenergic subtype contribution in bone vasculature. Tibiac were obtained from mongrel dogs, the nutrient artery was catheterized, and the bone was placed in an ex vivo perfusion apparatus at constant flow. Perfusion was accomplished using oxygenated Krebs-Ringer solution. A norepinephrine dose-response curve was obtained by using incremental single bolus doses. Each bone was perfused with a vasoactive drug at a standard physiologic dosage. After 30 min of perfusion, a second norepinephrine dose-response curve was generated. The degree of attenuation of the norepinephrine dose-response curve, as determined by the total area under the curve, was interpreted as the relaxation effect of the drug on the smooth muscle of the vascular bed. Prazosin (α1-receptor antagonist), rauwolszin (α2-receptor antagonist), propranolol (β-receptor antagonist), and diltiazem (calcium-entry inhibitor) were evaluated. Our data suggest that α1 and α2 adrenergic receptor antagonism results in a quantitatively similar attenuation of norepinephrine-induced vascular smooth muscle contraction. Calcium-entry antagonism produced less, but significant, attenuation of smooth muscle contractility. Beta-adrenergic receptor blockade yielded only a slight, although consistent, reduction in reactivity. Simple perfusion with Krebs-Ringer solution had no effect.
Persistent Identifierhttp://hdl.handle.net/10722/171057
ISSN
2015 Impact Factor: 2.807
2015 SCImago Journal Rankings: 1.464
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDean, MTen_US
dc.contributor.authorWood, MBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:01Z-
dc.date.available2012-10-30T06:12:01Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Orthopaedic Research, 1992, v. 10 n. 1, p. 104-111en_US
dc.identifier.issn0736-0266en_US
dc.identifier.urihttp://hdl.handle.net/10722/171057-
dc.description.abstractAn ex vivo canine tibia model was used to quantitate the specific adrenergic subtype contribution in bone vasculature. Tibiae were obtained from mongrel dogs, the nutrient artery was catheterized, and the bone was placed in an ex vivo perfusion apparatus at constant flow. Perfusion was accomplished using oxygenated Krebs-Ringer solution. A norepinephrine dose-response curve was obtained by using incremental single bolus doses. Each bone was perfused with a vasoactive drug at a standard physiologic dosage. After 30 min of perfusion, a second norepinephrine dose-response curve was generated. The degree of attenuation of the norepinephrine dose-response curve, as determined by the total area under the curve, was interpreted as the relaxation effect of the drug on the smooth muscle of the vascular bed. Prazosin (α1-receptor antagonist), rauwolszin (α2-receptor antagonist), propranolol (β-receptor antagonist), and diltiazem (calcium-entry inhibitor) were evaluated. Our data suggest that α1 and α2 adrenergic receptor antagonism results in a quantitatively similar attenuation of norepinephrine-induced vascular smooth muscle contraction. Calcium-entry antagonism produced less, but significant, attenuation of smooth muscle contractility. Beta-adrenergic receptor blockade yielded only a slight, although consistent, reduction in reactivity. | An ex vivo canine tibia model was used to quantitate the specific adrenergic subtype contribution in bone vasculature. Tibiac were obtained from mongrel dogs, the nutrient artery was catheterized, and the bone was placed in an ex vivo perfusion apparatus at constant flow. Perfusion was accomplished using oxygenated Krebs-Ringer solution. A norepinephrine dose-response curve was obtained by using incremental single bolus doses. Each bone was perfused with a vasoactive drug at a standard physiologic dosage. After 30 min of perfusion, a second norepinephrine dose-response curve was generated. The degree of attenuation of the norepinephrine dose-response curve, as determined by the total area under the curve, was interpreted as the relaxation effect of the drug on the smooth muscle of the vascular bed. Prazosin (α1-receptor antagonist), rauwolszin (α2-receptor antagonist), propranolol (β-receptor antagonist), and diltiazem (calcium-entry inhibitor) were evaluated. Our data suggest that α1 and α2 adrenergic receptor antagonism results in a quantitatively similar attenuation of norepinephrine-induced vascular smooth muscle contraction. Calcium-entry antagonism produced less, but significant, attenuation of smooth muscle contractility. Beta-adrenergic receptor blockade yielded only a slight, although consistent, reduction in reactivity. Simple perfusion with Krebs-Ringer solution had no effect.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.elsevier.com/locate/orthresen_US
dc.relation.ispartofJournal of Orthopaedic Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone And Bones - Blood Supplyen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshMicrocomputersen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshSoftwareen_US
dc.subject.meshSympatholytics - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshYohimbine - Pharmacologyen_US
dc.titleAntagonist drugs and bone vascular smooth muscleen_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.doi10.1002/jor.1100100113-
dc.identifier.pmid1727930-
dc.identifier.scopuseid_2-s2.0-0026599013en_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage104en_US
dc.identifier.epage111en_US
dc.identifier.isiWOS:A1992GX48200012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDean, MT=7201596044en_US
dc.identifier.scopusauthoridWood, MB=7403448994en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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