Endogenous nitric oxide in expired air: Effects of acute exercise in humans

Bauer, John; Wald, Jeffrey; Doran, Shawn D.; Soda, David M.

doi:10.1016/0024-3205(94)00522-2

Cited by 62 publications

(57 citation statements)

References 15 publications

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“…Exercise increased VNO in man (Persson et al 1993;Bauer et al 1994;Trolin et al 1994) and in the horses in the present study. Persson et al (1993) Bauer et al 1994).…”

supporting

confidence: 66%

“…Persson et al (1993) Bauer et al 1994). This species difference may be expected if, indeed, NO contributes to the regulation of pulmonary vascular tone in the horse because pulmonary vascular pressures in this species are significantly higher during exercise than other species, including man (Erickson et al 1990;West et al 1993;West & Mathieu-Costello, 1995 Nitric oxide and exercise in the horse Bauer et al (1994) bronchiectasis and sinus inversus, has been associated with a deficiency of NO in the paranasal sinuses (Lundberg et al 1995).…”

mentioning

confidence: 99%

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Nitric oxide and exercise in the horse.

Mills

Marlin

Demoncheaux

et al. 1996

The Journal of Physiology

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1. The effects of exercise on the production rate of nitric oxide (NO) in exhaled air (VNO) and 20 1 min-', respectively, and induced cyclical changes in the breathing pattern.4. Exercise induced a linear increase in VNO with work intensity to a maximum (428 1 + 31'6 pmol min-' kg-) which coincided with the maximal oxygen uptake for the horses (138 3 + 11 7 ml min-' kg-), although a further increase in VNO (779 3 + 38-4 pmol min-' kg-') occurred immediately after exercise. The changes in VNo correlated well with the tidal volume (r = 0-968; P < 0-01) and the haematocrit (r = 0-855; P < 0-01). 5. In the first 2 min of high intensity exercise, inhaled NO (80 p.p.m.) significantly (P < 0 05) reduced the pulmonary artery pressure: during the first minute, pulmonary artery pressure was 83-1 + 7-6 mmHg compared with a control value of 94 4 + 6-3 mmHg, and during the second minute, 84-2 + 7-1 mmHg compared with a control value of 98-4 + 4-7 mmHg.There were no other significant changes in cardiovascular or respiratory indices, including cardiac output, measured during exercise between control and inhaled NO tests. 6. The results show that exhaled NO is released from the airways of the horse and may contribute to the regulation of pulmonary vascular tone during exercise.

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“…Exercise increased VNO in man (Persson et al 1993;Bauer et al 1994;Trolin et al 1994) and in the horses in the present study. Persson et al (1993) Bauer et al 1994).…”

supporting

confidence: 66%

mentioning

confidence: 99%

Nitric oxide and exercise in the horse.

Mills

Marlin

Demoncheaux

et al. 1996

The Journal of Physiology

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“…13 Nevertheless, the level of NO during exhalation differs in various pathophysiologic conditions; for examples, it is increased in patients with asthma, 23,24 bronchiectasis, 25 systemic lupus erythematosus, 26 and liver cirrhosis. 27,28 NO levels were also found to increase with exercise, 29,30 during the mid menstrual cycle in women, 31 and during pregnancy. 32 Conversely, NO was reduced with ethanol ingestion.…”

Section: Discussionmentioning

confidence: 85%

Reduced production of nitric oxide during haemodialysis

Sumino

Sato

Sakamaki³

et al. 1999

J Hum Hypertens

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Objective: To examine the influence of systemic nitric oxide (NO) synthesis on blood pressure in patients with chronic renal failure undergoing haemodialysis, since nitric oxides are susceptible to renal excretion or are dialysed, a different indicator that is unaffected by renal function, such as the level of exhaled NO was evaluated. We examined the levels of the endogenous NO before and after a haemodialysis session. Design and methods: We evaluated the serum concentrations of nitrite/nitrate and the rate of nitric oxide release into exhaled air in 10 patients with hypertension who were receiving maintenance haemodialysis. Results: The serum concentrations of nitrite/nitrate before haemodialysis were significantly higher than those in 10 normal controls (183 ؎ 151 M vs 42 ؎ 17 M, P Ͻ 0.05). These levels decreased signifi-

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“…13 Exhaled NO levels have also been found to increase with exercise 14 and in response to orally administered L-arginine 15 and intravenously infused nitroglycerin. 16 Conversely, the exhaled NO level is decreased in patients with heart failure, 17 hypertension, 18 and acute respiratory distress syndrome.…”

Section: Sumino Et Al Enalapril Increases Exhaled Nitric Oxidementioning

confidence: 99%

Effect of Enalapril on Exhaled Nitric Oxide in Normotensive and Hypertensive Subjects

Sumino

Nakamura²,

Kanda³

et al. 2000

Hypertension

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Abstract-We investigated whether an angiotensin-converting enzyme (ACE) inhibitor increases the production of nitric oxide (NO) in exhaled air in normotensive and hypertensive subjects. In study 1, 8 normotensive male subjects received a single oral dose of enalapril (5 mg) or nitrendipine (10 mg) in a crossover manner. Exhaled air was collected at baseline, and at 2, 4, and 8 hours after administration of the drug. In study 2, 10 normotensive subjects (6 men and 4 women) and 10 hypertensive subjects (6 men and 4 women) received a single oral dose of enalapril (5 mg). Exhaled air was collected at baseline and at 2 and 4 hours after administration of the drug. In study 1, enalapril significantly increased the NO release rate from the lung in normotensive subjects (36.9Ϯ5.1 pmol/s at baseline versus 58.3Ϯ7.3 pmol/s at 4 hours, PϽ0.01). Nitrendipine did not change the NO release rate. In study 2, enalapril significantly increased the release of NO from the lung in normotensive subjects (40.4Ϯ6.0 pmol/s at baseline versus 70.3Ϯ11.4 pmol/s at 4 hours, PϽ0.01) but not in hypertensive subjects. ACE inhibition increased NO production from the lung in normotensive subjects but not in hypertensive patients. The reduction of angiotensin II production and/or the accumulation of bradykinin in the pulmonary tissue may be responsible for increased NO production in components of the lung, such as the pulmonary vascular endothelium, bronchial epithelial cells, macrophages, nasopharyngeal cells, and neurons. However, the effects of ACE inhibition on NO production from the lung differ between hypertensive subjects and normotensive subjects. Key Words: angiotensin Ⅲ bradykinin Ⅲ hypertension, essential Ⅲ nitric oxide E ndothelium-derived relaxing factor (EDRF) has been identified as nitric oxide (NO), a potent vasodilator. 1 The attenuated endothelium-dependent vasodilation in patients with essential hypertension 2 may be largely mediated by a decrease in the release or activity of NO. Decreased endothelial NO is considered to be either a cause or a consequence of hypertension.NO is a highly unstable substance with a plasma half-life of only a few seconds 3 ; therefore, its direct measurement is difficult, particularly in vivo. Endogenously produced NO is assessed by measuring the serum levels of NOx, the products of NO metabolism, or by measuring endogenous NO present in expired air. The presence of endogenous NO in exhaled air has been demonstrated in humans. 4 The cellular source of exhaled NO is not known, but it has been proposed that all NO synthase isoforms in the respiratory system contribute to NO release. 5 Therefore, the amount of NO in expired air is an appropriate indicator of endogenously produced NO in the lung. We recently developed a method for measuring NO in exhaled air. 6 Angiotensin-converting enzyme (ACE) inhibitors improve impaired endothelium-dependent vascular relaxation in rats, 7 but this effect of ACE inhibitors is not always demonstrated in humans. 8,9 However, it has not yet been established whether or...

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Endogenous nitric oxide in expired air: Effects of acute exercise in humans

Cited by 62 publications

References 15 publications

Nitric oxide and exercise in the horse.

Nitric oxide and exercise in the horse.

Reduced production of nitric oxide during haemodialysis

Effect of Enalapril on Exhaled Nitric Oxide in Normotensive and Hypertensive Subjects

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