The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia
Open accessAbstract
Acute hypoxic vasoconstriction and development of hypoxic pulmonary hypertension (PHTN) are unique properties of the pulmonary circulation. The pulmonary endothelium produces vasoactive factors, including nitric oxide (NO), that modify these phenomena. We tested the hypothesis that NO produced by endothelial nitric oxide synthase (eNOS) modulates pulmonary vascular responses to hypoxia using mice with targeted disruption of the eNOS gene (eNOS-/-). Marked PHTN was found in eNOS-/- mice raised in mild hypoxia when compared with either controls or eNOS-/- mice raised in conditions simulating sea level. We found an approximate twofold increase in partially and fully muscularized distal pulmonary arteries in eNOS-/- mice compared with controls. Consistent with vasoconstriction being the primary mechanism of PHTN, however, acute inhalation of 25 ppm NO resulted in normalization of RV pressure in eNOS-/- mice. In addition to studies of eNOS-/- mice, the dose-effect of eNOS was tested using heterozygous eNOS+/- mice. Although the lungs of eNOS+/- mice had 50% of normal eNOS protein, the response to hypoxia was indistinguishable from that of eNOS-/- mice. We conclude that eNOS-derived NO is an important modulator of the pulmonary vascular response to chronic hypoxia and that more than 50% of eNOS expression is required to maintain normal pulmonary vascular tone.
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
Hypertension in mice lacking the gene for endothelial nitric oxide synthase
Huang, P. L., Huang, Z., Mashimo, H., Bloch, K. D., Moskowitz, M. A., Bevan, J. A., & Fishman, M. C. (1995) · Nature · doi:10.1038/377239a0 · Cited by 2,070
Self-citationGiaid, A., & Saleh, D. (1995) · New England Journal of Medicine · doi:10.1056/nejm199507273330403 · Cited by 1,369
Elevated blood pressures in mice lacking endothelial nitric oxide synthase
Shesely, E. G., Maeda, N., Kim, H.-S., Desai, K. M., Krege, J. H., Laubach, V. E., Sherman, P. A., Sessa, W. C., & Smithies, O. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.23.13176 · Cited by 914
Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling.
Rudic, R. D., Shesely, E. G., Maeda, N., Smithies, O., Segal, S. S., & Sessa, W. C. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1699 · Cited by 821
Nitric oxide regulates basal systemic and pulmonary vascular resistance in healthy humans.
Stamler, J. S., Loh, E., Roddy, M. A., Currie, K. E., & Creager, M. A. (1994) · Circulation · doi:10.1161/01.cir.89.5.2035 · Cited by 516
Cornwell, T. L., Arnold, E., Boerth, N. J., & Lincoln, T. M. (1994) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.1994.267.5.c1405 · Cited by 455
Moroi, M., Zhang, L., Yasuda, T., Virmani, R., Gold, H. K., Fishman, M. C., & Huang, P. L. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1293 · Cited by 338
Self-citationLe Cras, T. D., Xue, C., Rengasamy, A., & Johns, R. A. (1996) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.1996.270.1.l164 · Cited by 254
Self-citationSteudel, W., Ichinose, F., Huang, P. L., Hurford, W. E., Jones, R. C., Bevan, J. A., Fishman, M. C., & Zapol, W. M. (1997) · Circulation Research · doi:10.1161/01.res.81.1.34 · Cited by 251
Self-citationSteudel, W., Scherrer-Crosbie, M., Bloch, K. D., Weimann, J., Huang, P. L., Jones, R. C., Picard, M. H., & Zapol, W. M. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2356 · Cited by 226
Self-citation
Cited by
Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension
Rabinovitch, M., Guignabert, C., Humbert, M., & Nicolls, M. R. (2014) · Circulation Research · doi:10.1161/circresaha.113.301141 · Cited by 1,029
Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications
Wu, L., & Wang, R. (2005) · Pharmacological Reviews · doi:10.1124/pr.57.4.3 · Cited by 962
Xu, Q., Bernardo, A., Walker, D., Kanegawa, T., Mahley, R. W., & Huang, Y. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.5476-05.2006 · Cited by 524
Pulmonary Arterial Hypertension: The Clinical Syndrome
Lai, Y.-C., Potoka, K. C., Champion, H. C., Mora, A. L., & Gladwin, M. T. (2014) · Circulation Research · doi:10.1161/circresaha.115.301146 · Cited by 402
Xu, W., Kaneko, F. T., Zheng, S., Comhair, S. A. A., Janocha, A. J., Goggans, T., Thunnissen, F. B. J. M., Farver, C., Hazen, S. L., Jennings, C., et al. (2004) · The FASEB Journal · doi:10.1096/fj.04-2317fje · Cited by 369
Metadata
- Authors
- Fagan, K. A., Fouty, B. W., Tyler, R. C., Morris, K. G., Hepler, L. K., Sato, K., LeCras, T. D., Abman, S. H., Weinberger, H. D., Huang, P. L., McMurtry, I. F., & Rodman, D. M.
- Venue
- Journal of Clinical Investigation
- Published
- 1999-01-15
- Volume
- 103
- Issue
- 2
- Pages
- 291-299
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2107821473
- Cited by
- 309
- References
- 22
- FWCI
- 17.20
- Type
- journal article
- Language
- en
- Open access
- bronze
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: The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia. https://app.cochat.ai/papers/10.1172/jci3862
- The paper
- Fagan, K. A., Fouty, B. W., Tyler, R. C., Morris, K. G., Hepler, L. K., Sato, K., LeCras, T. D., Abman, S. H., Weinberger, H. D., Huang, P. L., McMurtry, I. F., & Rodman, D. M. (1999). The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia. Journal of Clinical Investigation. https://doi.org/10.1172/jci3862
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.
