Investigation of PDE5 effect on NOS in nasal polyp pathophysiology.

[PURPOSE] Nasal polyps are masses resulting from chronic mucosal inflammation. Nitric oxide (NO) has recently attracted attention in nasal polyps as it plays an important role in both acute and chronic inflammation. One of the important mechanisms controlling NO production is phosphodiesterase (PDE) enzymes. The enzyme phosphodiesterase type 5 (PDE5) is an important regulator of cyclic guanosine 3'-5'-monophosphate (cGMP) signalling. PDE5 inhibitors increase intracellular cGMP concentration by inhibiting cGMP degradation and prolong NO signalling. NO is thought to cause nasal congestion because it increases microvascular permeability and causes mucosal oedema. The aim of our study was to investigate the role of PDE5, inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) in the pathophysiology of nasal polyps with mucosal oedema in histopathology.

[METHODS] Nasal mucosal tissues were obtained from 25 patients with nasal polyps who underwent endoscopic sinus surgery as the study group and 25 patients who underwent rhinoplasty as the control group. eNOS, iNOS and PDE5 levels were measured in nasal mucosal tissues.

[RESULTS] The mean age was 47.40 ± 16.33 years in the nasal polyp group and 35.44 ± 12.47 years in the normal group, and 64.0% (n = 16) of both groups were male. ELISA measurements showed that PDE5 levels were significantly decreased and iNOS and eNOS levels were significantly increased in the nasal polyp group compared with the control group. CONCLUSıON: This study suggest that iNOS, eNOS, and PDE5 may play important roles in the pathophysiology of nasal polyps.