Role of airway endogenous nitric oxide on lung function during and after exercise in mild asthma

2002 ◽  
Vol 93 (6) ◽  
pp. 1932-1938 ◽  
Author(s):  
Oscar E. Suman ◽  
Kenneth C. Beck
Keyword(s):  
Nitric Oxide ◽  
Cell Types ◽  
Constant Load ◽  
Forced Expiratory Volume ◽  
Mild Asthma ◽  
Airway Function ◽  
Endogenous Nitric Oxide ◽  
Slow Rise ◽  
Exercise Induced ◽  
Synthase Inhibitor

We hypothesized that nitric oxide (NO), a known mild bronchodilator that can be released by several cell types within pulmonary airways, might protect airways during exercise in asthmatic subjects. We studied 17 individuals with documented exercise-induced asthma (screening exercise evaluation) on 2 study days: after treatment with inhaled NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA; 2 ml of 25 mg/ml mist) and after treatment with saline vehicle. Pulmonary resistance (Rl, esophageal manometry) rose and forced expiratory volume in 1 s fell more after l-NMMA compared with saline treatment, suggesting a bronchoprotective role for NO at baseline. The rise in Rlseen after l-NMMA treatment was nearly completely reversed early in exercise, suggesting a non-NO-mediated bronchodilation. A slow rise in Rl during constant-load exercise and dramatic increase in Rl after exercise were the same on the 2 treatment days, indicating little role for NO in regulating airway function during and after exercise. We conclude that endogenous NO plays little role in regulating airway function during and after exercise in subjects with mild asthma.

Evaluation of pulmonary resistance and maximal expiratory flow measurements during exercise in humans

1999 ◽  
Vol 86 (4) ◽  
pp. 1388-1395 ◽  
Author(s):  
Kenneth C. Beck ◽  
Robert E. Hyatt ◽  
Panagiotis Mpougas ◽  
Paul D. Scanlon
Keyword(s):  
Vital Capacity ◽  
Normal Subjects ◽  
Forced Expiratory Volume ◽  
Pulmonary Resistance ◽  
Tidal Breathing ◽  
Flow Measurements ◽  
Airway Function ◽  
Minor Influence ◽  
Exercise Induced ◽  
Exercise In Humans

To evaluate methods used to document changes in airway function during and after exercise, we studied nine subjects with exercise-induced asthma and five subjects without asthma. Airway function was assessed from measurements of pulmonary resistance (Rl) and forced expiratory vital capacity maneuvers. In the asthmatic subjects, forced expiratory volume in 1 s (FEV1) fell 24 ± 14% and Rl increased 176 ± 153% after exercise, whereas normal subjects experienced no change in airway function (Rl−3 ± 8% and FEV1−4 ± 5%). During exercise, there was a tendency for FEV1 to increase in the asthmatic subjects but not in the normal subjects. Rl, however, showed a slight increase during exercise in both groups. Changes in lung volumes encountered during exercise were small and had no consistent effect on Rl. The small increases in Rl during exercise could be explained by the nonlinearity of the pressure-flow relationship and the increased tidal breathing flows associated with exercise. In the asthmatic subjects, a deep inspiration (DI) caused a small, significant, transient decrease in Rl 15 min after exercise. There was no change in Rl in response to DI during exercise in either asthmatic or nonasthmatic subjects. When percent changes in Rl and FEV1 during and after exercise were compared, there was close agreement between the two measurements of change in airway function. In the groups of normal and mildly asthmatic subjects, we conclude that changes in lung volume and DIs had no influence on Rl during exercise. Increases in tidal breathing flows had only minor influence on measurements of Rl during exercise. Furthermore, changes in Rl and in FEV1 produce equivalent indexes of the variations in airway function during and after exercise.

scholarly journals Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaoyu Liu ◽  
John Fassett ◽  
Yidong Wei ◽  
Yingjie Chen
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Farnesoid X Receptor ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Nitric Oxide Bioavailability

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.

scholarly journals Endogenous Nitric Oxide Synthase Inhibitor in Human Atheromatous Lesion

1997 ◽  
Vol 75 ◽  
pp. 55
Author(s):  
Hidehiro Matsuoka ◽  
Hiroshi Miyazaki ◽  
Seiya Katoh ◽  
Hideo Yasukawa ◽  
Michiaki Usui ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Oxide Synthase
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