Endothelium-dependent relaxation by tetraoctylammonium ions in rat isolated aortic rings.

Quaternary ammonium ions are common pharmacological blockers of K+ channels. This study examined the vasorelaxant effect of tetraoctylammonium ions (TOA+) in rat isolated aortic rings. TOA+ caused a concentration-dependent transient relaxation of endothelium-intact tissues. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 3x10(-5) M) or methylene blue (3 x 10(-6) M) or removal of the endothelium abolished the TOA+-induced relaxation. L-arginine (10(-3) M ) partially antagonized the effect of L-NAME. Glibenclamide (3x10(-6) M), charybdotoxin (CTX, 10(-7) M), indomethacin (10(-5) M), or atropine (3x10(-6) M) had no effect. Both TOA+ (10(-5) M)- and acetylcholine (ACh, 10(-5) M)-induced increase in tissue content of cyclic GMP was significantly attenuated by NG-nitro-L-arginine (L-NNA, 10(-4) M) and abolished in endothelium-denuded arteries. These results indicate that TOA+ induced endothelium-dependent relaxation which is likely mediated through nitric oxide but not other endothelium-derived factors. This relaxant action seems unique for TOA+ since other quaternary ammonium ions did not cause nitric oxide-dependent relaxation.