Effect of voltage-gated and capacitative calcium entry blockade on agonist-induced constriction of equine laminar blood vessels.
Abstract: 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.
Publication Date: 2007-07-04 PubMed ID: 17605607DOI: 10.2460/ajvr.68.7.722Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- Non-P.H.S.
Summary
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This research investigates how different types of calcium entry affect how horse blood vessels in the foot (laminar arteries and veins) constrict in response to different stimuli. Differences were also observed between responses of arteries vs veins.
Methodology
- The researchers conducted this study with 16 adult mixed-breed horses.
- Their methodology involved isolating the horses’ laminar arteries and veins and mounting them on small vessel myographs, which measure isometric tension, essentially the force produced during muscle contractions in the blood vessels.
- The scientists then observed how these isolated vessels reacted to different vasoconstrictor (blood vessel constricting) agents: phenylephrine, 5-hydroxytryptamine (5-HT), prostaglandin F(2) (PGF(2)), and endothelin-1 (ET-1).
- These agents were applied either in the presence of inhibitors that block calcium channels (diltiazem) and capacitative calcium entry (a peculiar form of calcium signaling) via trifluoromethylphenylimidazole, or without the presence of extracellular calcium (Ca2+).
Results
- The results in the absence of extracellular calcium were significant, with the responses of the vessels to various agents reduced by various degrees in both arteries and veins.
- However, the reductions were more drastic in arteries compared to veins, suggesting that calcium plays a more critical role in artery constriction.
- The specific calcium channel blocker (diltiazem) reduced the constrictive response of arteries to the vasoconstrictor agents, but didn’t affect the veins. This further emphasizes the significant role voltage-gated calcium entry might play in arterial contractions.
- Trifluoromethylphenylimidazole (which serves as an inhibitor of capacitative calcium entry) reduced the veins’ response to lower concentrations of certain agonists, but not their maximum responses. This indicates that capacitative calcium entry has a minor role in how these veins behave.
Conclusions
- The researchers concluded that the reliance on calcium for the contraction of these blood vessels varies between arteries and veins, as well as between different contractile stimuli.
- Extracellular calcium was found to be more prominent in the contraction mechanism of arteries than in veins.
- The part played by capacitative calcium entry in these contractions was deemed to be minor, especially for veins.
Cite This Article
APA
Peroni JF, Moore JN, Noschka E, Lewis TH, Lewis SJ, Robertson TP.
(2007).
Effect of voltage-gated and capacitative calcium entry blockade on agonist-induced constriction of equine laminar blood vessels.
Am J Vet Res, 68(7), 722-729.
https://doi.org/10.2460/ajvr.68.7.722 Publication
Researcher Affiliations
- Department of Physiology and Pharmacology, Institute of Comparative Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7389, USA.
MeSH Terms
- Adrenergic alpha-Agonists / pharmacology
- Animals
- Calcium / antagonists & inhibitors
- Calcium / metabolism
- Calcium Channel Blockers / pharmacology
- Diltiazem / pharmacology
- Dinoprost / pharmacology
- Endothelin-1 / pharmacology
- Hoof and Claw / blood supply
- Horses / physiology
- Imidazoles / pharmacology
- In Vitro Techniques
- Logistic Models
- Muscle, Smooth, Vascular / drug effects
- Muscle, Smooth, Vascular / metabolism
- Muscle, Smooth, Vascular / physiology
- Phenylephrine / pharmacology
- Serotonin / pharmacology
- Vasoconstriction / drug effects
Citations
This article has been cited 2 times.- Morgan RA, Keen JA, Walker BR, Hadoke PW. Vascular Dysfunction in Horses with Endocrinopathic Laminitis.. PLoS One 2016;11(9):e0163815.
- Menzies-Gow NJ, Wray H, Bailey SR, Harris PA, Elliott J. The effect of tumour necrosis factor-α and insulin on equine digital blood vessel function in vitro.. Inflamm Res 2014 Aug;63(8):637-47.
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