Effects of induction of capacitative calcium entry on equine laminar microvessels

Tom P. Robertson Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens, GA 30602-7389.

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John F. Peroni Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389.

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Stephen J. Lewis Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens, GA 30602-7389.

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James N. Moore Department of Physiology and Pharmacology, Institute of Comparative Medicine, University of Georgia, Athens, GA 30602-7389.
Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389.

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Abstract

Objective—To determine the effects of induction of capacitative Ca2+ entry on tone in equine laminar arteries and veins.

Sample Population—Laminar arteries and veins from 6 adult mixed-breed horses.

Procedure—Arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Capacitative Ca2+ entry was induced by incubating the vessels with the specific Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+- free physiologic salt solution. Capacitative Ca2+ entry–associated contractile responses were determined by the subsequent addition of 2mM Ca2+ to the solution bathing the vessels; in some experiments, either the voltage-gated Ca2+ blocker diltiazem (10µM) or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole (300µM) was added to the bathing solution 15 minutes prior to a second 2mM Ca2+ exposure. The Sr2+ permeability of the capacitative Ca2+ entry pathway in laminar vessels was assessed by exposing the vessels to 4mM Sr2+ after induction of capacitative Ca2+ entry with thapsigargin.

Results—Induction of capacitative Ca2+ entry elicited robust contractile responses in laminar veins but did not increase tone in laminar arteries. In laminar veins, capacitative Ca2+ entry–induced contractile responses were unaffected by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole, and were impermeable to Sr2+.

Conclusions and Clinical Relevance—Results indicated that induction of capacitative Ca2+ entry elicits vasoconstriction in equine laminar veins but not in laminar arteries and should therefore be considered a potential mechanism by which selective venoconstriction occurs in horses during the development of acute laminitis. (Am J Vet Res 2005;66:1877–1880)

Abstract

Objective—To determine the effects of induction of capacitative Ca2+ entry on tone in equine laminar arteries and veins.

Sample Population—Laminar arteries and veins from 6 adult mixed-breed horses.

Procedure—Arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Capacitative Ca2+ entry was induced by incubating the vessels with the specific Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+- free physiologic salt solution. Capacitative Ca2+ entry–associated contractile responses were determined by the subsequent addition of 2mM Ca2+ to the solution bathing the vessels; in some experiments, either the voltage-gated Ca2+ blocker diltiazem (10µM) or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole (300µM) was added to the bathing solution 15 minutes prior to a second 2mM Ca2+ exposure. The Sr2+ permeability of the capacitative Ca2+ entry pathway in laminar vessels was assessed by exposing the vessels to 4mM Sr2+ after induction of capacitative Ca2+ entry with thapsigargin.

Results—Induction of capacitative Ca2+ entry elicited robust contractile responses in laminar veins but did not increase tone in laminar arteries. In laminar veins, capacitative Ca2+ entry–induced contractile responses were unaffected by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole, and were impermeable to Sr2+.

Conclusions and Clinical Relevance—Results indicated that induction of capacitative Ca2+ entry elicits vasoconstriction in equine laminar veins but not in laminar arteries and should therefore be considered a potential mechanism by which selective venoconstriction occurs in horses during the development of acute laminitis. (Am J Vet Res 2005;66:1877–1880)

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