Evidence map›Paper›PMID 7560074›Full record

ArticleThe Journal of clinical investigation1995

Angiotensin converting enzyme expression is increased in small pulmonary arteries of rats with hypoxia-induced pulmonary hypertension.

N W Morrell, E N Atochina, K G Morris, S M Danilov, K R Stenmark

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 210 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Diagnostic and therapeutic precision in cardiovascular diseases in the neonatal intensive care.Journal of perinatology : official journal of the California Perinatal Association · 2025
    Review
  5. Biomarkers in COPD-Associated PH/CCP: Circulating Molecules and Cell-Intrinsic Marker.International journal of chronic obstructive pulmonary disease · 2025
    Review
  6. Review
  7. Systemic hemodynamics and pediatric lung disease: mechanistic links and therapeutic relevance.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  8. Review
  9. Article
  10. Molecular Pathways in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Neurohormonal modulation in pulmonary arterial hypertension.The European respiratory journal · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Targeting the renin-angiotensin signaling pathway in COVID-19: Unanswered questions, opportunities, and challenges.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

N W MorrellLung Developmental Biology Laboratory, University of Colorado Health Sciences Center, Denver 80262, USA.
E N Atochina
K G Morris
S M Danilov
K R Stenmark
University of Colorado Health · USInserm · FR

Funding

SCOR-LUNG BIOLOGY AND DISEASES IN INFANTS AND CHILDRENP50HL046481 · NHLBI · UNIVERSITY OF COLORADO DENVER · 1992 to 1996
–
NHLBI NIH HHS HL-14985NHLBI NIH HHS HL-46481
6 · The paper itself

Abstract

Previous studies suggest that while lung angiotensin converting enzyme (ACE) activity is reduced during chronic hypoxia, inhibitors of ACE attenuate hypoxic pulmonary hypertension. In an attempt to explain this paradox we investigated the possibility that whole lung ACE activity may not reflect local pulmonary vascular ACE expression. The experimental approach combined in vivo hemodynamic studies in control and chronically hypoxic rats, measurement of whole lung ACE activity, and evaluation of local pulmonary vascular ACE expression by in situ hybridization and immunohistochemistry. Total lung ACE activity was reduced to 50% of control activity by 5 d of hypoxia and remained low for the duration of the study. Immunohistochemistry showed a marked reduction of ACE staining in alveolar capillary endothelium. However, an increase in ACE staining was observed in the walls of small newly muscularized pulmonary arteries at the level of alveolar ducts and walls. In situ hybridization studies showed increased signal for ACE mRNA in the same vessels. Inhibition of ACE by captopril during chronic hypoxia attenuated pulmonary hypertension and markedly reduced distal muscularization of small pulmonary arteries. In addition, we demonstrated marked longitudinal variation in ACE expression along the normal pulmonary vasculature with the highest levels found in small muscular arteries associated with terminal and respiratory bronchioles. We conclude that local ACE expression is increased in the walls of small pulmonary arteries during the development of hypoxic pulmonary hypertension, despite a generalized reduction in alveolar capillary ACE expression, and we speculate that local arteriolar ACE may play a role in the vascular remodeling associated with pulmonary hypertension.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsHypertension, PulmonaryHypoxiaImmunohistochemistryIn Situ HybridizationKidneyMalePeptidyl-Dipeptidase APulmonary ArteryRatsRats, Sprague-DawleyRNA, MessengerAngiotensin-Converting Enzyme InhibitorsPeptidyl-Dipeptidase ARNA, Messenger

Identifiers

PMID7560074
PMCPMC185819
OpenAlexW2146149181

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.