Ascorbate elevates perfusion pressure in the bovine extraocular long posterior ciliary artery: role of endothelium-derived hyperpolarizing factor (EDHF)
Autor: | William S. Wilson, Alicia McGuckin, William Martin, Silvia Nelli, Vivian Wing Man Ho, Alison Stirrat |
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Rok vydání: | 2006 |
Předmět: |
medicine.medical_specialty
Endothelium-derived hyperpolarizing factor Endothelium Long posterior ciliary arteries Vasodilation Ascorbic Acid Ciliary Arteries Biological Factors medicine.artery Internal medicine medicine Potassium Channel Blockers Pressure Animals Vasoconstrictor Agents Pharmacology Dose-Response Relationship Drug Chemistry Ascorbic acid Intermediate-Conductance Calcium-Activated Potassium Channels Ciliary arteries Perfusion medicine.anatomical_structure Endocrinology Anesthesia 15-Hydroxy-11 alpha 9 alpha-(epoxymethano)prosta-5 13-dienoic Acid cardiovascular system Pyrazoles Cattle Endothelium Vascular circulatory and respiratory physiology Myograph |
Zdroj: | European journal of pharmacology. 534(1-3) |
ISSN: | 0014-2999 |
Popis: | Ascorbate blocks agonist-induced, endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation in the bovine perfused ciliary artery and this is associated with a rise in perfusion pressure. We now report the origins of this ascorbate-induced rise in perfusion pressure. In segments of ciliary artery perfused at 2.5 ml/min, the addition of ascorbate (10–150 μM) enhanced U46619-induced perfusion pressure. Ascorbate produced no enhancement in the absence of U46619, suggesting that its effects resulted not from a constrictor action but through removal of a tonic vasodilator influence. Experiments revealed the endothelial source of this vasodilator influence, and EDHF, but not nitric oxide or prostanoids, appeared to be involved. The ascorbate-induced enhancement of vasoconstrictor tone was not seen in a static myograph or in segments perfused at low rates of flow, but was seen at flow rates of 2.5 ml− 1 and above. We conclude that ascorbate augments vasoconstrictor tone through inhibition of flow-induced EDHF activity. |
Databáze: | OpenAIRE |
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