AI Article Synopsis
- The study investigates the functional expression of beta3-adrenoceptors (beta3-ARs) in equine digital veins (EDVs) and how their relaxation response is affected by endotoxin.
- Samples were taken from the forelimbs of 30 horses, with EDVs being isolated and tested for relaxation responses using various beta3-AR agonists in controlled conditions.
- Results indicated that while beta3-ARs promote relaxation in EDVs, their efficacy is reduced when exposed to endotoxin, suggesting that inflammatory responses may interfere with this mechanism, potentially due to changes in prostanoid production.
Article Abstract
Objective: To investigate the functional expression of beta3-adrenoceptors (beta3-ARs) in equine digital veins (EDVs) and to examine whether beta3-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 beta3-AR agonists (SR 58611A, ZD 2079, and ZM 215001).
Results: In intact EDVs, isoprenaline, SR 58611A, ZD 2079, and ZM 215001 induced concentration-dependent relaxation. Isoprenaline and SR 58611A-induced relaxations were reduced or unaffected by nadolol, respectively. In intact EDVs, SR 58611A-induced relaxation was significantly reduced in the presence of 2 microM ZM 215001 (used as a beta3-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: Beta3-adrenoceptors are functionally expressed in EDVs. Incubation in the presence of endotoxin, used as an in vitro model of laminitis, induced an alteration of beta-AR-mediated relaxations in EDVs, which could be the consequence of cyclooxygenase induction and subsequent prostanoid production.
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| http://dx.doi.org/10.2460/ajvr.2003.64.708 | DOI Listing |
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