Cardiovascular PharmacologyHydrogen peroxide as a mediator of vasorelaxation evoked by N-Oleoylethanolamine (cas 111-58-0) and anandamide in rat small mesenteric arteries

Add time:08/21/2019    Source:sciencedirect.com

Hydrogen peroxide (H2O2) has been shown to participate in endothelium-derived hyperpolarising factor (EDHF)-mediated mechanisms. Vasorelaxation to the endocannabinoid-like N-Oleoylethanolamine (cas 111-58-0) (OEA) and anandamide has been shown to be endothelium-dependent. Therefore, the principal aim was to investigate whether H2O2 plays a role in vasorelaxation to endocannabinoids in rat mesenteric arteries. We have also investigated the effects of catalase on endothelium-dependent relaxations and vascular responses to H2O2. First- (G1) and third- (G3) order branches of the superior mesenteric artery from male, Wistar rats were mounted in a wire myograph, contracted with methoxamine, and concentration–response curves to anandamide, OEA carbachol or H2O2, were constructed. The influence of nitric oxide production and H2O2 breakdown on these responses were then investigated using L-NAME (300 μM), and catalase (1000 U ml− 1) respectively. In G1 mesenteric arteries, vasorelaxations to carbachol and H2O2 were inhibited by L-NAME, but not by catalase. Responses to both anandamide and OEA were also unaffected by catalase. In G3 mesenteric arteries, endothelium-dependent relaxations to carbachol were modestly affected by L-NAME, unaffected by catalase alone, but their combination greatly inhibited vasorelaxation. Similarly, catalase inhibited vasorelaxation to anandamide and OEA, and combined treatment with L-NAME further reduced this response. In G1 mesenteric arteries, vasorelaxation to H2O2 is predominantly mediated by nitric oxide. We conclude that in G3 arteries H2O2 activity contributes towards EDHF-type responses and vasorelaxation to endocannabinoids, either directly or indirectly. Given the association between vascular pathophysiology and H2O2, these findings may provide a mechanism whereby disease states may influence responses to endocannabinoid and related mediators.

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