Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2537483 | European Journal of Pharmacology | 2006 | 7 Pages |
Abstract
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 mlâ 1 and above. We conclude that ascorbate augments vasoconstrictor tone through inhibition of flow-induced EDHF activity.
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Authors
Alison Stirrat, Silvia Nelli, Alicia McGuckin, Vivian Wing Man Ho, William S. Wilson, William Martin,