The effect of cooling on the contractility of equine digital small lamellar arteries: modulating role of the endothelium.
The equine hoof displays thermoregulatory functions, and the blood vessels lying under the hoof wall are temperature sensitive. The aim of this study was to investigate the effect of cooling on the contractile responses to α-adrenoceptor and 5-HT receptor stimulation in equine small lamellar arteries using wire myography. The role of the endothelium in the response mediated by 5-HT was also evaluated. Moderate cooling caused a reduction of the contraction induced by depolarizing Krebs solution (DKS, containing 118 mm KCl) and the maximal contraction caused by UK-14304 (α(2)-adrenoceptor agonist). The potency of methoxamine (α(1)-adrenoceptor agonist) was reduced by cooling [pD(2) (-log EC(50)) at 22°C, 5.7 (5.5-6.0) versus 30°C, 5.9 (5.7-6.1)]; however, the efficacy was maintained. The contractions evoked by sumatripan and α-methyl 5-HT (5-HT receptor agonists) were not modified by moderate cooling. In contrast, a cooling-enhanced contraction was observed in response to 5-HT [maximum response (E(max)) at 22°C, 213.2 ± 13% DKS versus 30°C, 179.9 ± 11% DKS]. Furthermore, this effect was more evident in endothelium-denuded lamellar arteries (E(max) at 22°C, 270.2 ± 26% DKS versus 30°C, 172.2 ± 20% DKS), suggesting a potential modulating role of the endothelium. The L-NAME/ibuprofen-resistant relaxation in response to carbachol was reduced by cooling in small lamellar arteries precontracted with 5-HT but not phenylephrine. Therefore, a moderate reduction of temperature modulates the reactivity of small lamellar arteries by enhancing the 5-HT-mediated contraction, but inhibits the α-adrenoceptor-mediated response. Furthermore, the endothelium of these blood vessels may play an important role in preventing excessive vasoconstriction in response to 5-HT and maintaining digital blood flow in cool environmental temperatures.
Zerpa
Hector
H
Department of Veterinary Basic Sciences, Royal Veterinary College, University of London, London, UK.
Berhane
Yoel
Y
Elliott
Jonathan
J
Bailey
Simon R
SR
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology; D001833:Body Temperature Regulation; D003080:Cold Temperature; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006724:Hoof and Claw / Q000098:blood supply*; D006736:Horses; D008297:Male; D009213:Myography; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D012039:Regional Blood Flow; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D017366:Serotonin Receptor Agonists; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D019001:Nitric Oxide Synthase