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- Publisher Website: 10.1002/jor.1100100113
- Scopus: eid_2-s2.0-0026599013
- PMID: 1727930
- WOS: WOS:A1992GX48200012
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Article: Antagonist drugs and bone vascular smooth muscle
Title | Antagonist drugs and bone vascular smooth muscle |
---|---|
Authors | |
Keywords | Adrenergics Antagonist Bone vasculature Free vascularized graft Osseous microcirculation Vasodilation |
Issue Date | 1992 |
Publisher | John 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? |
Abstract | An 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 Identifier | http://hdl.handle.net/10722/171057 |
ISSN | 2023 Impact Factor: 2.1 2023 SCImago Journal Rankings: 0.886 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Dean, MT | en_US |
dc.contributor.author | Wood, MB | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:12:01Z | - |
dc.date.available | 2012-10-30T06:12:01Z | - |
dc.date.issued | 1992 | en_US |
dc.identifier.citation | Journal Of Orthopaedic Research, 1992, v. 10 n. 1, p. 104-111 | en_US |
dc.identifier.issn | 0736-0266 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171057 | - |
dc.description.abstract | An 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.language | eng | en_US |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.elsevier.com/locate/orthres | en_US |
dc.relation.ispartof | Journal of Orthopaedic Research | en_US |
dc.subject | Adrenergics | - |
dc.subject | Antagonist | - |
dc.subject | Bone vasculature | - |
dc.subject | Free vascularized graft | - |
dc.subject | Osseous microcirculation | - |
dc.subject | Vasodilation | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Bone And Bones - Blood Supply | en_US |
dc.subject.mesh | Diltiazem - Pharmacology | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Dose-Response Relationship, Drug | en_US |
dc.subject.mesh | Microcomputers | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular - Drug Effects | en_US |
dc.subject.mesh | Norepinephrine - Pharmacology | en_US |
dc.subject.mesh | Prazosin - Pharmacology | en_US |
dc.subject.mesh | Software | en_US |
dc.subject.mesh | Sympatholytics - Pharmacology | en_US |
dc.subject.mesh | Vasoconstriction - Drug Effects | en_US |
dc.subject.mesh | Yohimbine - Pharmacology | en_US |
dc.title | Antagonist drugs and bone vascular smooth muscle | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1002/jor.1100100113 | - |
dc.identifier.pmid | 1727930 | - |
dc.identifier.scopus | eid_2-s2.0-0026599013 | en_US |
dc.identifier.volume | 10 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 104 | en_US |
dc.identifier.epage | 111 | en_US |
dc.identifier.isi | WOS:A1992GX48200012 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Dean, MT=7201596044 | en_US |
dc.identifier.scopusauthorid | Wood, MB=7403448994 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0736-0266 | - |