Nitrite

About: Nitrite is a research topic. Over the lifetime, 15425 publications have been published within this topic receiving 484581 citations.

Simultaneous measurement of nitrite and nitrate levels as indices of nitric oxide release in the cerebellum of conscious rats.

Abstract: We examined the modulation of nitric oxide production in vivo by measuring levels of nitrite (NO 2 - ) and nitrate (NO 3 - ) in the dialysate of the cerebellum in conscious rats, by using an in vivo brain microdialysis technique. The levels of both NO 2 - and NO 3 - were decreased by the intraperitoneal injection of NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, whereas N G -nitro-D-arginine methyl ester had no effect. L-Arginine by itself increased NO 2 - and NO 3 - levels and diminished the reduction of their levels caused by NG-nitro-L-arginine methyl ester. Direct infusion of L-glutamate, N-methyl-D-aspartate, or KCI into the cerebellum through a dialysis probe resulted in an increase in NO 2 - and/or NO 3 - levels. The effects of N-methyl-D-aspartate and KCI were dependent on extracellular calcium. Furthermore, the stimulatory effects of L-glutamate and N-methyl-D-aspartate were inhibited by N G -nitro-L-arginine methyl ester and (±)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP), an N-methyl-D-aspartate receptor antagonist. These results suggest that NO 2 - and NO 3 - levels may be related to nitric oxide production in vivo.

Salivary contribution to exhaled nitric oxide

Abstract: Dietary and metabolic nitrate is distributed from the blood to the saliva by active uptake in the salivary glands, and is reduced to nitrite in the oral cavity by the action of certain bacteria. Since it has been reported that nitric oxide may be formed nonenzymatically from nitrite this study aimed to determine whether salivary nitrite could influence measurements of exhaled NO. Ten healthy subjects fasted overnight and ingested 400 mg potassium nitrate, equivalent to approximately 200 g spinach. Exhaled NO and nasal NO were regularly measured with a chemiluminescence technique up to 3 h after the ingestion. Measurements of exhaled NO were performed with a single-breath procedure, standardized to a 20-s exhalation, at a flow of 0.15 L x s(-1), and oral pressure of 8-10 cmH2O. Values of NO were registered as NO release rate (pmol x s(-1)) during the plateau of exhalation. Exhaled NO increased steadily over time after nitrate load and a maximum was seen at 120 min (77.0+/-15.2 versus 31.2+/-3.0 pmol x s(-1), p<0.01), whereas no increase was detected in nasal NO levels. Salivary nitrite concentrations increased in parallel; at 120 min there was a four-fold increase compared with baseline (1.56+/-0.44 versus 0.37+/-0.09 mM, p<0.05). The nitrite-reducing conditions in the oral cavity were also manipulated by the use of different mouthwash procedures. The antibacterial agent chlorhexidine acetate (0.2%) decreased NO release by almost 50% (p<0.01) 90 min after nitrate loading and reduced the preload control levels by close to 30% (p<0.05). Sodium bicarbonate (10%) also reduced exhaled NO levels, but to a somewhat lesser extent than chlorhexidine acetate. In conclusion, salivary nitric oxide formation contributes to nitric oxide in exhaled air and a large intake of nitrate-rich foods before the investigation might be misinterpreted as an elevated inflammatory activity in the airways. This potential source of error and the means for avoiding it should be considered in the development of a future standardized method for measurements of exhaled nitric oxide.