Key result
Patients with primary pulmonary hypertension had significantly lower mean 12-hour excretion of (15)N-nitrite and (15)N-nitrate compared to controls (57.2 vs. 229.1 nmol/mmol creatinine, p < 0.01).
Why the study?
Is NOS-dependent whole body NO production decreased in patients with primary pulmonary hypertension compared to age-matched controls?
Case-Control (n=10)
Is NOS-dependent whole body NO production decreased in patients with primary pulmonary hypertension compared to age-matched controls?
Absolute Event Rate: 57.2% vs 229.1%
p-value: p=< 0.01
Patients with primary pulmonary hypertension exhibit impaired basal NOS-dependent whole body NO production or excess NO metabolism compared to healthy controls.
May reflect impaired NO production in primary pulmonary hypertension; hypothesis-generating for NOS-targeted therapies.
Impaired pulmonary release of nitric oxide (NO) is one of the characteristic phenotypic changes of vascular cells in pulmonary hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with primary pulmonary hypertension. NOS-dependent whole body NO production was assessed by giving an intravenous infusion of L-[(15)N](2)-arginine (50 micromol/min for 30 min) and measuring isotopic urinary enrichment of (15)N-nitrite and (15)N-nitrate. Four female patients with no signs of infection were recruited and compared with 6 age-matched control subjects. Mean 12-hour excretion of (15)N-nitrite and (15)N-nitrate in the total urine over 36 h was smaller in patients than in control subjects (57.2 +/- 27.6 vs. 229.1 +/- 65.2 nmol/mmol creatinine, p < 0.01, Mann-Whitney U test, respectively). Neither mean 12-hour excretion of (14)N-nitrite and (14)N-nitrate (51.6 +/- 10.0 vs. 72.4 +/- 10.0 micromol/mmol creatinine, p = 0.3) nor glomerular filtration rates (84.5 +/- 15.8 vs. 129.7 +/- 16.0 ml/min, p = 0.1) were different between patients and control subjects. Our results suggest that either basal NOS-dependent whole body NO production is impaired or excess NO metabolism occurs in patients with primary pulmonary hypertension.
No takes yet. Share an insight, caveat, or question.
Demoncheaux et al. (2005) conducted a case-control in Primary pulmonary hypertension (n=10). Primary pulmonary hypertension vs. Age-matched control subjects was evaluated on Mean 12-hour excretion of (15)N-nitrite and (15)N-nitrate in the total urine over 36 h (p=< 0.01). Patients with primary pulmonary hypertension had significantly lower mean 12-hour excretion of (15)N-nitrite and (15)N-nitrate compared to controls (57.2 vs. 229.1 nmol/mmol creatinine, p < 0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: