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  • Author or Editor: Veronique Bucas x
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Objective—To investigate the functional expression of β3-adrenoceptors (β3-ARs) in equine digital veins (EDVs) and to examine whether β3-AR relaxation was altered in EDVs incubated with endotoxin.

Sample Population—Forelimbs obtained from 30 horses.

Procedure—Forelimbs were obtained from horses in an abattoir. Equine digital veins were carefully removed from distal portions of the forelimbs. Rings of dissected EDVs were mounted in 5-mL organ baths to record isometric tension in the presence of various β3-AR agonists (SR 58611A, ZD 2079, and ZM 215001).

Results—In intact EDVs, isoprenaline, SR 58611A, ZD 2079, and ZM 215001 induced concentrationdependent relaxation. Isoprenaline and SR 58611Ainduced relaxations were reduced or unaffected by nadolol, respectively. In intact EDVs, SR 58611Ainduced relaxation was significantly reduced in the presence of 2µM ZM 215001 (used as a β3-AR antagonist). In endothelium-denuded EDVs or intact EDVs in the presence of a nitric oxide synthase inhibitor, isoprenaline and SR 58611A-induced relaxations were significantly decreased. The endothelium-independent relaxation to SR 58611A was significantly inhibited in the presence of ZM 215001. In endotoxin-treated EDV, isoprenaline- and SR 58611A-induced relaxations were significantly reduced. In these conditions, cycloheximide (a protein synthesis inhibitor) and ibuprofen (a cyclooxygenase inhibitor) restored the relaxant response to SR 58611A.

Conclusions and Clinical Relevance—β3-Adrenoceptors are functionally expressed in EDVs. Incubation in the presence of endotoxin, used as an in vitro model of laminitis, induced an alteration of β-ARmediated relaxations in EDVs, which could be the consequence of cyclooxygenase induction and subsequent prostanoid production. (Am J Vet Res 2003;64:708–714)

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in American Journal of Veterinary Research