title: Effects of induction of capacitative calcium entry on equine laminar microvessels.
abstract: OBJECTIVE
  To determine the effects of induction of capacitative Ca2+ entry on tone in equine laminar arteries and veins.
  
  
  METHODS
  Laminar arteries and veins from 6 adult mixed-breed horses.
  
  
  METHODS
  Arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Capacitative Ca2+ entry was induced by incubating the vessels with the specific Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+-free physiologic salt solution. Capacitative Ca2+ entry-associated contractile responses were determined by the subsequent addition of 2mM Ca2+ to the solution bathing the vessels; in some experiments, either the voltage-gated Ca2+ blocker diltiazem (10microM) or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole (300microM) was added to the bathing solution 15 minutes prior to a second 2mM Ca2+ exposure. The Sr2+ permeability of the capacitative Ca2+ entry pathway in laminar vessels was assessed by exposing the vessels to 4mM Sr2+ after induction of capacitative Ca2+ entry with thapsigargin.
  
  
  RESULTS
  Induction of capacitative Ca2+ entry elicited robust contractile responses in laminar veins but did not increase tone in laminar arteries. In laminar veins, capacitative Ca2+ entry-induced contractile responses were unaffected by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole, and were impermeable to Sr+.
  
  
  CONCLUSIONS
  Results indicated that induction of capacitative Ca2+ entry elicits vasoconstriction in equine laminar veins but not in laminar arteries and should therefore be considered a potential mechanism by which selective venoconstriction occurs in horses during the development of acute laminitis.
authors.affiliation: Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens 30602-7389, USA.
authors.forename: Tom P
authors.initials: TP
authors.lastname: Robertson
authors.forename: John F
authors.initials: JF
authors.lastname: Peroni
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Lewis
authors.forename: James N
authors.initials: JN
authors.lastname: Moore
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005552:Forelimb / Q000098:blood supply; D006724:Hoof and Claw / Q000098:blood supply; D006736:Horses / Q000502:physiology*; D066298:In Vitro Techniques; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009213:Myography / Q000662:veterinary; D013324:Strontium / Q000502:physiology; D019284:Thapsigargin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014680:Veins / Q000187:drug effects / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D019284:Thapsigargin; D004110:Diltiazem; D002118:Calcium; D013324:Strontium