title: Predisposition for venoconstriction in the equine laminar dermis: implications in equine laminitis.
abstract: Equine laminitis is a crippling condition associated with a variety of systemic diseases. Although it is apparent that the prodromal stages of laminitis involve microvascular dysfunction, little is known regarding the physiology of this vasculature. The aim of the present study was to determine the relative responses of equine laminar arteries and veins to the vasoconstrictor agonists phenylephrine (1 nM-10 microM), 5-HT (1 nM-10 microM), PGF2alpha (1 nM-100 microM), and endothelin-1 (1 pM-1 microM). We have determined that laminar veins were more sensitive, with respect to the concentration of agonist required to initiate a contractile response and to achieve EC(50), for all agonists tested. EC50 values, for veins and arteries, respectively, were 84+/-7 vs. 688+/-42 nM for phenylephrine, 35+/-6 vs. 224+/-13 nM for 5-HT, 496+/-43 nM vs. 3.0+/-0.6 microM for PGF2alpha, and 467+/-38 pM vs. 70.6+/-6.4 nM for endothelin-1. Moreover, when expressed as a percentage of the response to a depolarizing stimulus (80 mM potassium), the maximal contractile response of laminar veins exceeded that for the laminar arteries for each agonist. These results indicate that there may be a predisposition for venoconstriction within the vasculature of the equine digit. While this physiological predisposition for venoconstriction may be important in the regulation of blood flow during exercise, it also may help to explain why laminitis can result from a variety of pathological systemic conditions.
authors.affiliation: Dept. of Physiology and Pharmacology, College of Veterinary Medicine, Univ. of Georgia, Athens, Georgia, 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: Megan E
authors.initials: ME
authors.lastname: Grafton
authors.forename: Maria
authors.initials: M
authors.lastname: Aceves-Avila
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Lewis
authors.forename: Tom P
authors.initials: TP
authors.lastname: Robertson
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology; D015984:Causality; D020405:Dermis / Q000098:blood supply* / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology; D019332:Endothelin-1 / Q000494:pharmacology; D005534:Foot Diseases / Q000209:etiology / Q000503:physiopathology / Q000662:veterinary*; D006724:Hoof and Claw / Q000098:blood supply*; D006734:Horse Diseases / Q000209:etiology* / Q000503:physiopathology; D006736:Horses / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D012701:Serotonin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014680:Veins / Q000187:drug effects / Q000503:physiopathology
chemical_list: D019332:Endothelin-1; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D012701:Serotonin; D015237:Dinoprost; D011188:Potassium