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Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension.
J Vasc Res. 2005 Mar-Apr; 42(2):133-6.JV

Abstract

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.

Authors+Show Affiliations

Division of Clinical Sciences (South), University of Sheffield, Royal Hallamshire Hospital, Sheffield, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15665548

Citation

Demoncheaux, Eric A G., et al. "Decreased Whole Body Endogenous Nitric Oxide Production in Patients With Primary Pulmonary Hypertension." Journal of Vascular Research, vol. 42, no. 2, 2005, pp. 133-6.
Demoncheaux EA, Higenbottam TW, Kiely DG, et al. Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension. J Vasc Res. 2005;42(2):133-6.
Demoncheaux, E. A., Higenbottam, T. W., Kiely, D. G., Wong, J. M., Wharton, S., Varcoe, R., Siddons, T., Spivey, A. C., Hall, K., & Gize, A. P. (2005). Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension. Journal of Vascular Research, 42(2), 133-6.
Demoncheaux EA, et al. Decreased Whole Body Endogenous Nitric Oxide Production in Patients With Primary Pulmonary Hypertension. J Vasc Res. 2005;42(2):133-6. PubMed PMID: 15665548.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decreased whole body endogenous nitric oxide production in patients with primary pulmonary hypertension. AU - Demoncheaux,Eric A G, AU - Higenbottam,Tim W, AU - Kiely,David G, AU - Wong,Ju-Ming, AU - Wharton,Simon, AU - Varcoe,Richard, AU - Siddons,Tom, AU - Spivey,Alan C, AU - Hall,Keith, AU - Gize,Andy P, Y1 - 2005/01/21/ PY - 2004/08/05/received PY - 2004/11/22/accepted PY - 2005/1/25/pubmed PY - 2005/5/12/medline PY - 2005/1/25/entrez SP - 133 EP - 6 JF - Journal of vascular research JO - J. Vasc. Res. VL - 42 IS - 2 N2 - 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. SN - 1018-1172 UR - https://www.unboundmedicine.com/medline/citation/15665548/Decreased_whole_body_endogenous_nitric_oxide_production_in_patients_with_primary_pulmonary_hypertension_ L2 - https://www.karger.com?DOI=10.1159/000083502 DB - PRIME DP - Unbound Medicine ER -