Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 100: 759-763, 2006. First published November 3, 2005; doi:10.1152/japplphysiol.00794.2005
8750-7587/06 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
100/3/759    most recent
00794.2005v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Peroni, J. F.
Right arrow Articles by Robertson, T. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Peroni, J. F.
Right arrow Articles by Robertson, T. P.

Predisposition for venoconstriction in the equine laminar dermis: implications in equine laminitis

John F. Peroni,2 James N. Moore,1,2 Erik Noschka,2 Megan E. Grafton,2 Maria Aceves-Avila,2 Stephen J. Lewis,1 and Tom P. Robertson1

1Department of Physiology and Pharmacology, Institute of Comparative Medicine, and 2Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, Georgia

Submitted 5 July 2005 ; accepted in final form 2 November 2005

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 µM), 5-HT (1 nM–10 µM), PGF2{alpha} (1 nM–100 µM), and endothelin-1 (1 pM–1 µM). 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 EC50, 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 µM for PGF2{alpha}, 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.

equine laminar arteries; veins



Address for reprint requests and other correspondence: T. Robertson, Dept. of Physiology and Pharmacology, College of Veterinary Medicine, Univ. of Georgia, Athens, Georgia, GA 30602–7389 (e-mail: troberts{at}vet.uga.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.