Montelukast exerts no acute direct effect on NO synthases.

摘要: The cysteinyl leukotrienes (CysLTs) LTC(4), LTD(4) and LTE(4) are potent proinflammatory lipid mediators that play a central role in inflammation, contraction remodelling of airways observed asthmatics. Montelukast, competitive inhibitor the leukotriene-1 (CysLT(1)) receptor attenuates asthmatic airway remodelling. As number studies have shown montelukast reduced exhaled nitric oxide (NO) levels, marker inflammation correlates with severity asthma, we investigated whether or not direct inhibition NO synthase (NOS) by takes place. In an ex vivo rat lung perfusion ventilation model NOS-dependent vasodilation effect after lipopolysaccharide (LPS) infusion was assessed without montelukast. Functional organ bath using isolated aortic rings from same species aimed to assess effects on inducible endothelial NOS isoenzymes (i- eNOS) as well iNOS expression. Neuronal (nNOS) field stimulated rabbit corpus cavernosum, human enzyme activity for potential inhibition. Montelukast failed cause vasoconstriction LPS challenged lung, inhibit i- eNOS expression species. Also assays nNOS cavernosum gave no evidence physiological supraphysiological concentrations up 10(-4)M. We therefore conclude has acute action. Its is probably indirectly mediated modulation inflammation.