Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

NO in the lung

S Adnot1, B Raffestin, S Eddahibi

  • 1Dèpartement de Physiologie et INSERM U296, Hôpital Henri Mondor, Crèteil, France.

Respiration Physiology
|August 1, 1995
PubMed
Summary
This summary is machine-generated.

Nitric oxide (NO) plays a vital role in lung function, regulating blood vessels and airways. Impaired NO production contributes to pulmonary hypertension, but inhaled NO therapy can help.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Lung mTOR activation leads to lung fibrosis or emphysema via senescence of specific lung cells.

Scientific reports·2026
Same author

[Senescence of the pulmonary endothelial cells: VEGF, a new target in pulmonary pathologies and aging].

Revue des maladies respiratoires·2025
Same author

[Discussion about the presentation: "Cell senescence, a new target for respiratory viral infections: from influenza virus to SARS-CoV-2"].

Bulletin de l'Academie nationale de medecine·2023
Same author

[Cell senescence, a new target for respiratory viral infections: From influenza virus to SARS-CoV-2].

Bulletin de l'Academie nationale de medecine·2023
Same author

Axial stretch-dependent cation entry in dystrophic cardiomyopathy: Involvement of several TRPs channels.

Cell calcium·2016
Same author

Inactivation of p53 Is Sufficient to Induce Development of Pulmonary Hypertension in Rats.

PloS one·2015
Same journal

Braking of expiratory airflow in obese pigs during wakefulness and sleep.

Respiration physiology·2002
Same journal

Arousal response to hypoxia in newborn mice.

Respiration physiology·2002
Same journal

The oxygen gain of diving insects.

Respiration physiology·2002
Same journal

The role of endothelin-1 in strain-related susceptibility to develop hypoxic pulmonary hypertension in rats.

Respiration physiology·2002
Same journal

Active glottal closure during anoxic gasping in lambs.

Respiration physiology·2002
Same journal

Avian intrapulmonary chemoreceptor discharge rate is increased by anion exchange blocker 'DIDS'.

Respiration physiology·2002
See all related articles

Area of Science:

  • Pulmonary medicine
  • Cardiovascular physiology
  • Cellular signaling

Background:

  • Nitric oxide (NO) is produced by various lung cells, mediating paracrine signaling.
  • Endothelial NO causes vasodilation in pulmonary vessels, while airway NO relaxes smooth muscle.
  • Activated macrophages produce NO during immune responses.

Purpose of the Study:

  • To explore the multifaceted roles of nitric oxide (NO) in pulmonary physiology and pathology.
  • To understand NO's involvement in normal lung function and its dysregulation in pulmonary hypertension.
  • To highlight the therapeutic potential of exogenous NO in lung diseases.

Main Methods:

  • Literature review of NO's cellular sources and functions in the lung.
  • Analysis of NO's role in pulmonary circulation, airway function, and immune responses.

Related Experiment Videos

  • Examination of NO's involvement in chronic hypoxia-induced pulmonary hypertension.
  • Review of inhaled NO therapy for pulmonary hypertension and lung injury.

    • Main Results:

    • NO from endothelial cells, epithelial cells, nerve endings, and macrophages influences lung function.
    • In healthy lungs, NO promotes vasodilation, inhibits vasoconstriction and platelet adhesion, and regulates smooth muscle and extracellular matrix.
    • Impaired endothelial NO production in chronic hypoxia exacerbates pulmonary hypertension.
    • Exogenous NO selectively dilates pulmonary vessels and is a therapeutic agent.

    Conclusions:

    • Nitric oxide is crucial for maintaining normal pulmonary circulation and airway function.
    • Dysfunctional NO signaling contributes significantly to the pathogenesis of pulmonary hypertension.
    • Inhaled nitric oxide represents a valuable therapeutic strategy for managing pulmonary hypertension and improving oxygenation in lung injury.