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The role of nitric oxide in the responses of equine digital veins to vasodilator and vasoconstrictor agents.
Abstract: Isolated equine digital veins were examined in vitro to study the importance of the endothelium in the responses to both vasodilator and vasoconstrictor agents and to characterise the endothelial-derived mediators involved. Carbachol (Cch; 1 microM) and bradykinin (Bk; 1 nM) caused relaxation of U44069-induced tone by 79.5 +/- 0.35% and 73.7 +/- 4.0% respectively. Mechanical removal of the endothelium completely prevented relaxant responses to Cch and to Bk showing they were mediated by the endothelium. Treatment of veins with NG-nitro-L-arginine methyl ester (L-NAME; 30 and 300 microM) inhibited vasorelaxant responses to both Cch and Bk whereas the cyclooxygenase inhibitor, ibuprofen (10 microM) had no inhibitory effect. The inhibitory action of L-NAME on the relaxations produced by Cch was partly reversed by L-arginine (3 and 10 mM). Cch-relaxations were potentiated in the presence of super oxide dismutase (15 units/ml) and inhibited by methylene blue (10 microM). The vasorelaxant effects of ATP (0.01 microM to 0.1 mM) were not dependent on the presence of the endothelium and the selective P2y receptor agonist, 2-methylthio-ATP proved to be ineffective as a vasodilator. Removal of the endothelium did not enhance the vasoconstrictor effects of the alpha 1 adrenoceptor agonist phenylephrine (0.01 microM to 0.1 mM) and treatment with L-NAME (300 microM) did not change the vasoconstrictor responses to 5-HT (1 nM to 10 microM) or the alpha 2 adrenoceptor agonist BHT-920 (1 nM to 1 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
Publication Date: 1994-09-01 PubMed ID: 7988541DOI: 10.1111/j.2042-3306.1994.tb04407.xGoogle Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This research studies the role of nitric oxide in the reactions of horse veins to substances that cause constriction and dilation. It shows that nitric oxide seems to be the main mediator regulating these reactions, affecting how the veins respond to both types of substances.
Understanding Endothelial Responses
The researchers studied isolated horse veins in lab conditions to assess the importance of the endothelial layer (the inner lining of blood vessels) in response to substances promoting dilation (vasodilators) and constriction (vasoconstrictors) of blood vessels. Two such substances, Carbachol and Bradykinin, were used in the study:
- Both substances showed strong dilation effect on the veins.
- When the endothelium was physically removed, these substances had no effect, proving their action was indeed mediated by this layer.
Role of Nitric Oxide
The study then looked at the role of Nitric Oxide, a gaseous signaling molecule known to relax blood vessels:
- The researchers used a chemical called L-NAME that inhibits the production of nitric oxide.
- When this inhibitor was applied, the vasodilation effect of both Carbachol and Bradykinin was significantly decreased.
- This confirms that nitric oxide plays a crucial role in the relaxation response of the horse veins.
Involvement of Other Substances
The researchers also explored other substances for their potential effects:
- They used ibuprofen, known to inhibit cyclooxygenase, an enzyme involved in the inflammation process, but found it had no impact on the relaxation responses.
- ATP, a molecule carrying energy within cells, was found to cause vasorelaxation independently of the endothelium.
- Using a selective P2y receptor agonist (a substance that can initiate a physiological response when combined with a receptor), they found that it was not effective as a vasodilator.
Deleting Endothelium and Vasoconstrictor Effects
The researchers examined the potential enhancement of vasoconstrictor effects following the removal of the endothelium:
- When the endothelium was removed, there was no change in the strength of the vasoconstriction caused by the α1-adrenoceptor agonist phenylephrine.
- L-NAME, which inhibits nitric oxide, did not alter the vasoconstrictor responses of 5-HT or the α2-adrenoceptor agonist BHT-920.
Cite This Article
APA
Elliott J, Bryant CE, Soydan J.
(1994).
The role of nitric oxide in the responses of equine digital veins to vasodilator and vasoconstrictor agents.
Equine Vet J, 26(5), 378-384.
https://doi.org/10.1111/j.2042-3306.1994.tb04407.x Publication
Researcher Affiliations
- Department of Veterinary Basic Sciences, Royal Veterinary College, London, UK.
MeSH Terms
- Adenosine Triphosphate / pharmacology
- Animals
- Arginine / analogs & derivatives
- Arginine / pharmacology
- Bradykinin / pharmacology
- Carbachol / pharmacology
- Dose-Response Relationship, Drug
- Drug Interactions
- Endothelium, Vascular / drug effects
- Endothelium, Vascular / physiology
- Hindlimb / blood supply
- Horses / physiology
- Ibuprofen / pharmacology
- In Vitro Techniques
- NG-Nitroarginine Methyl Ester
- Nitric Oxide / antagonists & inhibitors
- Nitric Oxide / physiology
- Nitroprusside / pharmacology
- Phenylephrine / pharmacology
- Vasoconstrictor Agents / pharmacology
- Vasodilator Agents / pharmacology
- Veins / drug effects
- Veins / physiology
Citations
This article has been cited 3 times.- 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.
- Pawson P, Reid J, Nolan AM. The role of nitric oxide in the responses of the ovine digital artery to vasoactive agents and modification of these responses by endotoxin and cytokines. Br J Pharmacol 2000 May;130(1):109-17.
- Menzel JE, Kolarz G. Modulation of nitric oxide synthase activity by ibuprofen. Inflammation 1997 Aug;21(4):451-61.
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