Role of Nitric Oxide and Prostaglandin Systems in Lithium Modulation of Acetylcholine Vasodilation

Bahareh Rahimzadeh-Rofouyi | Banafsheh Afsharimani | Leila Moezi | Farzad Ebrahimi | Shahram Ejtemaei Mehr | Tajmah Mombeini | Mohammad Hosein Ghahremani | Ahmad R Dehpour

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URL :   http://research.shahed.ac.ir/WSR/WebPages/Report/PaperView.aspx?PaperID=1459
Date :  2007/12/22
Publish in :    Journal of Cardiovascular Pharmacology
DOI :  https://doi.org/10.1097/fjc.0b013e318153f262

Keywords :Nitric, Prostaglandin, systems, Lithium, Modulation, Acetylcholine, Vasodilation

Abstract :

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The mechanism of lithium action, an effective treatment for bipolar disease, is still unknown. The present study examined the role of nitric oxide (NO) and prostaglandin systems in lithium modulation of acetylcholine in mesenteric vascular bed of rats by cannulating superior mesenteric artery. Acetylcholine (ACh) or sodium nitroprusside was injected under constant controlled flow induced by phenylephrine; therefore, changes in perfusion pressure reflect changes in resistance. Although 0.5 mM or 1 mM lithiumpretreatment of vascular bed causes reduction inACh-response, 1.5 mM lithium induced no changes and 2 and 2.5 mM lithium potentiated ACh-induced mesenteric vascular bed relaxation compared to control group. Pretreatment of vascular bed with L-NAME or indomethacin decreased ACh-induced relaxation in 2 concentrations of 0.5 and 2 mM of lithium. The vasorelaxation response to sodium nitroprusside, the NO donor, was not different among lithium groups (0.5 and 2 mM) and controls. In conclusion, there is a dual modulation of endothelium-dependent relaxation, including an inhibitory effect at lower dose and a stimulating effect at higher dose of lithium in rat mesenteric vascular bed. NO synthesis or cyclooxygenase inhibition decreased vasorelaxation in both lower and higher doses of lithium, suggesting a role for NO and prostaglandin in this effect.