Intracavernosal pressure responses to sodium nitrite

Abstract

Till recently nitrite and nitrate were considered as inert biological end products of nitric oxide (NO) metabolism. However, studies in experimental animals and human subjects have shown that nitrite is reduced back to NO with significant vasodilator activity. The vadsoilatory effect of sodium nitrite in the corpus cavernosum (erectile function) has not yet been determined, and therefore was investigated. The erectile responses were evaluated by measuring intracavernosal pressure (ICP) with a 27 gauge needle placed in the crura. Intracavernosal (IC) injections of sodium nitrite (10 ‐ 100 µmol/kg) increased ICP in a dose‐dependent manner. The increases in pressure ranged from 5 to 50 mm Hg and were similar to responses elicited by IC injection of SNP. Maximum increases in ICP in response to sodium nitrite and SNP were similar to increases in pressure observed upon electrical stimulation of the corporal nerve. The IC injections of acetylcholine induced smaller increases in ICP than sodium nitrite or SNP. The IC injections of sodium nitrate however did not have any significant vasodilator effect. The results indicate that nitrite is converted to NO causing vasodilation and increases in cavernosal blood flow and erection in the rat. Additionally, it suggests that nitrite reductase activity is present in the corpora cavernousum of the rat and is consistent with the hypothesis that nitrite represents a storage form of NO.