Effect of voltage-gated and capacitative calcium entry blockade on agonist-inducted construction of equine laminar blood vessels
Date
2007
Authors
Peroni, J.
Moore, J.
Noschka, E.
Lewis, T.
Lewis, S.
Robertson, T.
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Journal article
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American Journal of Veterinary Research, 2007; 68(7):722-729
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John F. Peroni, James N. Moore, Erik Noschka, Tristan H. Lewis, Stephen J. Lewis, Tom P. Robertson
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Abstract
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 F2α (PGF2α), 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 PGF2α 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 PGF2α. 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.
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