| pubmed-article:7853773 | pubmed:abstractText | There is increasing evidence that nitric oxide (NO) plays a role in the regulation of airway and vascular smooth muscle tone, pulmonary microvascular permeability, and host defense. However, it remains uncertain whether NO is actually released from airway mucosa. We therefore directly measured NO concentrations in the perfusate of rabbit tracheal mucosal surface, with an NO-selective electrode. The electrode was made of Pt/Ir alloy coated with a three-layered membrane that consisted of KCl, No-selective silicone resin, and a normal silicone membrane. Termination of tracheal perfusion with Krebs-Henseleit solution increased the electrical current derived from oxidation of NO at the electrode, and reperfusion rapidly decreased the current to the baseline value. Addition of L-NG-arginine methylester (L-NAME, 10(-3) M) to the perfusate decreased NO release, but D-NAME had no effect. Subsequent addition of L-arginine (10(-3) M) reversed the inhibition by L-NAME and greatly increased NO release above the baseline value. Histochemical staining to reveal NADPH diaphorase activity in the tracheal tissue showed a strong blue reaction mainly in the epithelial cells. These results suggest that NO is continuously released in the airway mucosal surface, probably from the epithelial cells rich in NO synthase. | lld:pubmed |
