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Effect of voltage-gated and capacitative calcium entry blockade on agonist-induced constriction of equine laminar blood vessels.

OBJECTIVE
To characterize the relative contributions of voltage-gated and capacitative Ca(2+) 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(2) (PGF(2)), and endothelin-1 (ET-1) either in the absence of extracellular Ca(2+) or in the presence of the voltage-gated Ca(2+) channel inhibitor diltiazem or the putative inhibitor of capacitative Ca(2+) entry, trifluoromethylphenylimidazole.


RESULTS
In the absence of extracellular Ca(2+), maximal responses of veins to 5-HT, phenylephrine, ET-1 and PGF(2) 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(2).


CONCLUSIONS AND CLINICAL RELEVANCE
Results suggested that the contribution of extracellular Ca(2+) to laminar vessel contractile responses differs between arteries and veins and also between contractile agonists, voltage-gated Ca(2+) entry is more predominant in laminar arteries than in veins, and capacitative Ca(2+) entry has a minor role in agonist-induced contractile responses of laminar veins.