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Objective—To characterize the relative contributions of voltage-gated and capacitative Ca2+ entry to agonist-induced contractions of equine laminar arteries and veins.

Animals—16 adult mixed-breed horses.

Procedures—Laminar arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Concentration-response curves were obtained for the vasoconstrictor agonists phenylephrine, 5-hydroxytryptamine (5-HT), prostaglandin F (PGF), and endothelin-1 (ET-1) either in the absence of extracellular Ca2+ or in the presence of the voltage-gated Ca2+ channel inhibitor diltiazem or the putative inhibitor of capacitative Ca2+ entry, trifluoromethylphenylimidazole.

Results—In the absence of extracellular Ca2+, maximal responses of veins to 5-HT, phenylephrine, ET-1 and PGF were reduced by 80%, 50%, 50%, and 45%, respectively; responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 95%, 90%, and 20%, respectively. Although diltiazem did not affect the maximal responses of veins to any agonist, responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 40%, 50%, and 27%, respectively. Trifluoromethylphenylimidazole did not affect maximal responses of veins, but did reduce their contractile responses to low concentrations of ET-1 and PGF.

Conclusions and Clinical Relevance—Results suggested that the contribution of extracellular Ca2+ to laminar vessel contractile responses differs between arteries and veins and also between contractile agonists, voltage-gated Ca2+ entry is more predominant in laminar arteries than in veins, and capacitative Ca2+ entry has a minor role in agonist-induced contractile responses of laminar veins.

Full access
in American Journal of Veterinary Research


Objective—To provide insights into the role of prostaglandin F (PGF) in the developmental stages of laminitis induced in horses by ingestion of black walnut heartwood extract (BWHE).

Sample Population—10 adult mixed-breed horses.

Procedures—Horses were separated into 2 groups and were euthanatized at 12 hours after placebo (water) administration (control horses) or after BWHE administration and development of Obel grade 1 laminitis. Blood samples were obtained to determine plasma PGF concentrations hourly for the first 4 hours and subsequently every 2 hours after substance administration. Laminar arteries and veins were isolated, and responses to increasing concentrations of PGF were measured before and after preincubation of blood vessels with prostanoid and thromboxane receptor antagonists SQ 29,548, SC-19220, and AH 6809.

Results—Plasma PGF concentrations increased in horses given BWHE; the WBC count decreased concurrently. In control horses, PGF was a potent contractile agonist for laminar veins but not for laminar arteries. In horses given BWHE, PGF was similarly selective for laminar veins; however, the magnitude of PGF-induced venoconstriction was less than that in control horses. After preincubation with SQ 29,548, laminar veins from control horses responded to PGF with a small degree of dilation, whereas laminar veins from horses given BWHE did not.

Conclusions and Clinical Relevance—PGF may play a role in the inflammatory and vascular dysfunction associated with the prodromal stages of laminitis. Prostanoids such as PGF may be viable targets for the prevention of acute laminitis in horses.

Full access
in American Journal of Veterinary Research