The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Role of Nitric Oxide in the Pathogenesis of Chronic Pulmonary Hypertension
Abstract
Chronic pulmonary hypertension is a serious complication of a number of chronic lung and heart diseases. In addition to vasoconstriction, its pathogenesis includes injury to the peripheral pulmonary arteries leading to their structural remodeling. Increased pulmonary vascular synthesis of an endogenous vasodilator, nitric oxide (NO), opposes excessive increases of intravascular pressure during acute pulmonary vasoconstriction and chronic pulmonary hypertension, although evidence for reduced NO activity in pulmonary hypertension has also been presented. NO can modulate the degree of vascular injury and subsequent fibroproduction, which both underlie the development of chronic pulmonary hypertension. On one hand, NO can interrupt vascular wall injury by oxygen radicals produced in increased amounts in pulmonary hypertension. NO can also inhibit pulmonary vascular smooth muscle and fibroblast proliferative response to the injury. On the other hand, NO may combine with oxygen radicals to yield peroxynitrite and other related, highly reactive compounds. The oxidants formed in this manner may exert cytotoxic and collagenolytic effects and, therefore, promote the process of reparative vascular remodeling. The balance between the protective and adverse effects of NO is determined by the relative amounts of NO and reactive oxygen species. We speculate that this balance may be shifted toward more severe injury especially during exacerbations of chronic diseases associated with pulmonary hypertension. Targeting these adverse effects of NO-derived radicals on vascular structure represents a potential novel therapeutic approach to pulmonary hypertension in chronic lung diseases.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1
Forsythe, J. A., Jiang, B.-H., Iyer, N. V., Agani, F., Leung, S. W., Koos, R. D., & Semenza, G. L. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.9.4604 · Cited by 3,981
Appetite-suppressant drugs and the risk of primary pulmonary hypertension
Abenhaim, L., Moride, Y., Brenot, F., Rich, S., Benichou, J., Kurz, X., Higenbottam, T., Oakley, C., Wouters, E., Aubier, M., et al. (1996) · New England Journal of Medicine · doi:10.1056/nejm199608293350901 · Cited by 1,162
Sessa, W. C., Pritchard, K., Seyedi, N., Wang, J., & Hintze, T. H. (1994) · Circulation Research · doi:10.1161/01.res.74.2.349 · Cited by 934
The biology of nitrogen oxides in the airways
Gaston, B., Drazen, J. M., Loscalzo, J., & Stamler, J. S. (1994) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.149.2.7508323 · Cited by 918
Ignarro, L. J., Fukuto, J. M., Griscavage, J. M., Rogers, N. E., & Byrns, R. E. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.8103 · Cited by 856 · cited 1×
“Plasma concentration of the NO end-oxidation product nitrate (157) is elevated in congenital heart disease patients with high flow pulmonary hypertension (361, 383).”
Lee, P. J., Jiang, B.-H., Chin, B. Y., Iyer, N. V., Alam, J., Semenza, G. L., & Choi, A. K. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.9.5375 · Cited by 782
Clancy, R. M., Leszczynska-Piziak, J., & Abramson, S. B. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115929 · Cited by 686
High nitric oxide production in human paranasal sinuses
Lundberg, J. O. N., Farkas-Szallasi, T., Weitzberg, E., Rinder, J., Lidholm, J., Änggåard, A., Hökfelt, T., Lundberg, J. M., & Alving, K. (1995) · Nature Medicine · doi:10.1038/nm0495-370 · Cited by 628
THE PATHOPHYSIOLOGICAL ROLE OF PEROXYNITRITE IN SHOCK, INFLAMMATION, AND ISCHEMIA-REPERFUSION INJURY
Szabó, C. (1996) · Shock · doi:10.1097/00024382-199608000-00001 · Cited by 481
Nitric oxide, an autocrine regulator of wound fibroblast synthetic function
Schäffer, M. R., Efron, P. A., Thornton, F. J., Klingel, K., Gross, S. S., & Barbul, A. (1997) · The Journal of Immunology · doi:10.4049/jimmunol.158.5.2375 · Cited by 260
Cited by
PDE5 inhibitors – pharmacology and clinical applications 20 years after sildenafil discovery
Andersson, K. (2018) · British Journal of Pharmacology · doi:10.1111/bph.14205 · Cited by 445
Inhaled Nitric Oxide Therapy in Adults
Griffiths, M. J. D., & Evans, T. W. (2005) · New England Journal of Medicine · doi:10.1056/nejmra051884 · Cited by 398
Regulation of the Pulmonary Circulation in the Fetus and Newborn
Gao, Y., & Raj, J. U. (2010) · Physiological Reviews · doi:10.1152/physrev.00032.2009 · Cited by 345
Zhao, Y.-Y., Zhao, Y. D., Mirza, M. K., Huang, J. H., Potula, H.-H. S. K., Vogel, S. M., Brovkovych, V., Yuan, J. X.-J., Wharton, J., & Malik, A. B. (2009) · Journal of Clinical Investigation · doi:10.1172/jci33338 · Cited by 275
Casey, D. B., Badejo, A. M., Dhaliwal, J. S., Murthy, S. N., Hyman, A. L., Nossaman, B. D., & Kadowitz, P. J. (2009) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00543.2008 · Cited by 61
Metadata
- Authors
- Hampl, V., & Herget, J.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2000-01-10
- Volume
- 80
- Issue
- 4
- Pages
- 1337-1372
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W1880313810
- Cited by
- 248
- References
- 11
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Role of Nitric Oxide in the Pathogenesis of Chronic Pulmonary Hypertension. https://app.cochat.ai/papers/10.1152/physrev.2000.80.4.1337
- The paper
- Hampl, V., & Herget, J. (2000). Role of Nitric Oxide in the Pathogenesis of Chronic Pulmonary Hypertension. Physiological Reviews. https://doi.org/10.1152/physrev.2000.80.4.1337
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.