Effect of voltage-gated and capacitative calcium entry blockade on agonist-inducted construction of equine laminar blood vessels

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.