<scp>l</scp>-Arginine Increases Exhaled Nitric Oxide in Normal Human Subjects

Kharitonov, Sergei A.; Lübec, Gert; Lubec, Barbara; Hjelm, M.; Barnes, Peter J.

doi:10.1042/cs0880135

Cited by 151 publications

(102 citation statements)

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“…L-arginine, the substrate for enzymatic NO synthesis, has been shown to increase exhaled NO in a dose-dependent manner when taken orally [42], or infused intravenously [23]. This increase seems to take place primarily in the upper airways [23].…”

Section: Drugsmentioning

confidence: 99%

Nitric oxide in exhaled air

Lundberg¹,

Weitzberg²,

Lundberg³

et al. 1996

Eur Respir J

137

112

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Much interest is now being focused on measurements of nitric oxide (NO) in exhaled air. In healthy subjects exhaled NO seems to originate mainly in the nasal airways, whereas the contribution from the lower respiratory tract is low.In certain inflammatory airway disorders, the excretion of NO into the airways is altered resulting in changes in the levels of NO in exhaled air. New techniques have been developed to measure NO release at different levels of the airways: asthmatics show increased orally-exhaled NO levels, whereas patients with cystic fibrosis or Kartagener' 's syndrome exhibit a marked reduction in nasal release of NO. It has been suggested that measurements of exhaled NO may be clinically useful in noninvasive diagnosis and monitoring of inflammatory airway diseases.To further evaluate the potential clinical usefulness of measurement of exhaled NO, it is vital to explore how airway NO production is normally regulated and what factors influence airway NO excretion.

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Section: Drugsmentioning

confidence: 99%

Nitric oxide in exhaled air

Lundberg¹,

Weitzberg²,

Lundberg³

et al. 1996

Eur Respir J

137

112

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“…We found that glutathione infusion completely prevented hyperglycemiainduced hemodynamic changes and that L-arginine superimposed with ongoing hyperglycemia completely normalized the hemodynamic parameters as well as the baroreflex activity. The evidence for increased release of NO during systemic administration of L-arginine is based on elevation of some indexes of NO synthesis or degradation such as plasma citrulline and cGMP levels (22), urinary nitrate and nitrite (21), and exhaled NO (23). Moreover, similar doses of D-arginine, which is not used for endogenous NO synthesis (24), or L-lysine, which uses the same cationic amino acid transport system as L-arginine (25), have no effect on hyperglycemiainduced vascular changes, at least in normal subjects (7).…”

Section: Conclusion -mentioning

confidence: 99%

Hemodynamic effects of acute hyperglycemia in type 2 diabetic patients.

et al. 2000

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Abbreviations: dBP, diastolic blood pressure; HR, heart rate; MBP, mean blood pressure; NO, nitric oxide; sBP, systolic blood pressure; SqT, squatting test; SqTs, squatting sympathetic ratio; SqTv, squatting vagal ratio.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Hemodynamic Effects of Acute Hyperglycemia in Type 2 Diabetic PatientsOBJECTIVE -The aim of the present study was to evaluate the hemodynamic effects of acute hyperglycemia in type 2 diabetic patients and to see whether these effects are related to changes in nitric oxide (NO) availability.RESEARCH DESIGN AND METHODS -Twenty newly diagnosed complication-free diet-treated type 2 diabetic patients participated in the study. All patients underwent 3 hyperglycemic glucose clamps in random order: 1) the control study was performed with plasma glucose clamped at 18 mmol/l for 2 h; 2) the octreotide study with plasma insulin blocked at basal levels during the clamp; and 3) the L-arginine study with L-arginine (1 g/min) infused during the last 30 min of the clamp. A group of 8 patients also underwent a glutathione infusion (600 mg as an intravenous bolus followed by 5 mg/min infusion) during the clamp.RESULTS -During hyperglycemia, there were significant increments of systolic (sBP) (from 115.5 ± 9.1 to 120.3 ± 8.2 mmHg, P Ͻ 0.01) and diastolic (dBP) (from 70.3 ± 7.8 to 79.7 ± 5.3 mmHg, P Ͻ 0.01) blood pressure, as well as heart rate (from 75.2 ± 7.8 to 80.8 ± 5.4 beats/min, P Ͻ 0.01) and plasma catecholamines (P Ͻ 0.05). Squatting ratios, a measure of the baroreflex activity, significantly deteriorated after hyperglycemia (P Ͻ 0.01). The infusion of octreotide, used to avoid the possible confounding influence of insulin, did not change the hemodynamic effects of hyperglycemia. Glutathione, a free radical scavenger, completely prevented the vascular effects of hyperglycemia. L-Arginine produced a fall in sBP and dBP to baseline values and normalized squatting ratios.CONCLUSIONS -Acute hyperglycemia in newly diagnosed type 2 diabetic patients causes significant hemodynamic changes that are independent of endogenous insulin and are prevented by glutatione and reversed by L-arginine, suggesting an interference with endogenous NO availability. These observations could help explain the adverse cardiovascular effects of hyperglycemic spikes.

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“…l-Arg is a safe therapy (Perrine et al, 1994) that has demonstrated the capacity to decrease platelet aggregation (Adams et al, 1995) and reverse endothelial dysfunction (Lerman et al, 1998) in other disease processes and it may represent a new therapeutic intervention in SCD. NO x levels were shown to increase after oral l-Arg supplementation in healthy subjects (Kharitonov et al, 1995). We undertook a study to determine whether oral l-Arg increases NO x production in patients with SCD.…”

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confidence: 99%

Arginine therapy: a novel strategy to induce nitric oxide production in sickle cell disease

Morris¹,

Kuypers²,

Larkin³

et al. 2000

Br J Haematol

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To determine the effects of l‐arginine (l‐Arg) supplementation on nitric oxide metabolite (NOx) production, oral l‐Arg was given to normal controls, sickle cell disease (SCD) patients at steady state and SCD patients hospitalized with a vaso‐occlusive crisis (VOC). l‐Arg (0·1 g/kg) increased NOx formation by 18·8 ± 68% in normal controls, whereas steady‐state SCD patients demonstrated a paradoxical decrease in NOx of −16·7 ± 4% (P = 0·004). In contrast, patients with VOC demonstrated a dramatic increase in NOx production by +77·7 ± 103%, a response that was dose dependent. l‐Arg appears to be the rate‐limiting step in NOx production during VOC. Oral arginine may therefore benefit SCD patients by inducing an increase in NO production during VOC.

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l-Arginine Increases Exhaled Nitric Oxide in Normal Human Subjects

Cited by 151 publications

References 0 publications

Nitric oxide in exhaled air

Nitric oxide in exhaled air

Hemodynamic effects of acute hyperglycemia in type 2 diabetic patients.

Arginine therapy: a novel strategy to induce nitric oxide production in sickle cell disease

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