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.


METHODS
16 adult mixed-breed horses.


METHODS
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
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.
Peroni
John F
JF
Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA.
Moore
James N
JN
Noschka
Erik
E
Lewis
Tristan H
TH
Lewis
Stephen J
SJ
Robertson
Tom P
TP
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D015237:Dinoprost / Q000494:pharmacology; D019332:Endothelin-1 / Q000494:pharmacology; D006724:Hoof and Claw / Q000098:blood supply*; D006736:Horses / Q000502:physiology*; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D016015:Logistic Models; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D010656:Phenylephrine / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D019332:Endothelin-1; D007093:Imidazoles; D010656:Phenylephrine; D012701:Serotonin; D015237:Dinoprost; D004110:Diltiazem; D002118:Calcium