Lithium decreased endothelium-mediated, but not nonadrenergic noncholinergic, relaxation of guinea pig corpus cavernosum in vitro: a role for nitrergic system.

Lithium causes erectile dysfunction in patients but its mechanism is yet unknown. The aim of our study was to verify the effect of acute lithium administration on the nonadrenergic noncholinergic (NANC)- and endothelium-mediated relaxation of guinea pig isolated corpus cavernosum. Although lithium (0.5, 1, and 5mm) had no effect on the neurogenic relaxations, it significantly (P<0.001) attenuated the relaxant responses to acetylcholine in a concentration-dependent manner. Combination of low concentration of lithium (0.5mm) with either 0.1 or 1μm l-NAME significantly (P<0.001) reduced the endothelium-mediated relaxation. Although the Nitric oxide (NO) precursor l-arginine at 1mm did not alter the relaxant responses to acetylcholine in control strips, it improved the inhibition by lithium (1mm) of relaxant responses to acetylcholine. Sodium nitroprusside (SNP; 10nm-1mm) produced similar concentration-dependent relaxations in both groups. Our experiments indicated that lithium can result in impairment of the NO-mediated endothelium-dependent but not NANC relaxation of guinea pig corpus cavernosum.