title: Effect of voltage-gated and capacitative calcium entry blockade on agonist-induced constriction of equine laminar blood vessels.
abstract: OBJECTIVE
  To characterize the relative contributions of voltage-gated and capacitative Ca(2+) entry to agonist-induced contractions of equine laminar arteries and veins.
  
  
  METHODS
  16 adult mixed-breed horses.
  
  
  METHODS
  Laminar arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Concentration-response curves were obtained for the vasoconstrictor agonists phenylephrine, 5-hydroxytryptamine (5-HT), prostaglandin F(2) (PGF(2)), and endothelin-1 (ET-1) either in the absence of extracellular Ca(2+) or in the presence of the voltage-gated Ca(2+) channel inhibitor diltiazem or the putative inhibitor of capacitative Ca(2+) entry, trifluoromethylphenylimidazole.
  
  
  RESULTS
  In the absence of extracellular Ca(2+), maximal responses of veins to 5-HT, phenylephrine, ET-1 and PGF(2) were reduced by 80%, 50%, 50%, and 45%, respectively; responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 95%, 90%, and 20%, respectively. Although diltiazem did not affect the maximal responses of veins to any agonist, responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 40%, 50%, and 27%, respectively. Trifluoromethylphenylimidazole did not affect maximal responses of veins, but did reduce their contractile responses to low concentrations of ET-1 and PGF(2).
  
  
  CONCLUSIONS
  Results suggested that the contribution of extracellular Ca(2+) to laminar vessel contractile responses differs between arteries and veins and also between contractile agonists, voltage-gated Ca(2+) entry is more predominant in laminar arteries than in veins, and capacitative Ca(2+) entry has a minor role in agonist-induced contractile responses of laminar veins.
authors.affiliation: Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA.
authors.forename: John F
authors.initials: JF
authors.lastname: Peroni
authors.forename: James N
authors.initials: JN
authors.lastname: Moore
authors.forename: Erik
authors.initials: E
authors.lastname: Noschka
authors.forename: Tristan H
authors.initials: TH
authors.lastname: Lewis
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Lewis
authors.forename: Tom P
authors.initials: TP
authors.lastname: Robertson
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D015237:Dinoprost / Q000494:pharmacology; D019332:Endothelin-1 / Q000494:pharmacology; D006724:Hoof and Claw / Q000098:blood supply*; D006736:Horses / Q000502:physiology*; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D016015:Logistic Models; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D010656:Phenylephrine / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D019332:Endothelin-1; D007093:Imidazoles; D010656:Phenylephrine; D012701:Serotonin; D015237:Dinoprost; D004110:Diltiazem; D002118:Calcium