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

Lessons from genetically engineered animal models. IV. Nitric oxide synthase gene knockout mice.

H Mashimo1, R K Goyal

  • 1Department of Veteran Affairs Medical Center, West Roxbury 02132, Massachusetts, USA.

The American Journal of Physiology
|October 12, 1999
PubMed
Summary

Nitric oxide synthase (NOS) knockout mice reveal distinct roles for neuronal (nNOS), endothelial (eNOS), and inducible (iNOS) nitric oxide in neurotransmission, blood flow, and inflammation. Life-long deficiency causes specific physiological consequences in each mouse model.

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

Sustainable diets and functional foods for the prevention of cardio-metabolic diseases and sustainable development goals of the UNO. An international consensus of scientific statement of the international college of nutrition and 28th world congress on clinical nutrition, Bogor, Indonesia.

BMC cardiovascular disorders·2026
Same author

Morphology and electrical conductivity of carbon-coated Nickel reinforced high-performance polymer nanocomposites.

Nanotechnology·2024
Same author

Poly(ether-sulfone)/MWCNT nanocomposites manufactured by powder metallurgy route and their dynamic mechanical properties.

Nanotechnology·2024
Same author

High electromagnetic interference shielding of poly(ether-sulfone)/multi-walled carbon nanotube nanocomposites fabricated by an eco-friendly route.

Nanotechnology·2020
Same author

Volumetric laser endomicroscopy and its application to Barrett's esophagus: results from a 1,000 patient registry.

Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus·2019
Same author

Surgical pleth index: prospective validation of the score to predict moderate-to-severe postoperative pain.

British journal of anaesthesia·2019

Area of Science:

  • Physiology
  • Biochemistry
  • Pharmacology

Background:

  • Nitric oxide (NO) is a critical signaling molecule involved in numerous biological functions.
  • Three primary nitric oxide synthase (NOS) isoforms—neuronal (nNOS), endothelial (eNOS), and inducible (iNOS)—exhibit distinct tissue distributions and functions.
  • Conventional pharmacological tools struggle to differentiate NOS isoforms or model chronic NO depletion.

Purpose of the Study:

  • To elucidate the specific physiological roles of NO produced by nNOS, eNOS, and iNOS.
  • To investigate the consequences of life-long deficiency of each NOS isoform using knockout mouse models.
  • To identify compensatory mechanisms and redundant pathways in NO signaling.

Main Methods:

  • Generation and analysis of nNOS, eNOS, and iNOS knockout mice.

Related Experiment Videos

  • Assessment of physiological functions including neurotransmission, blood flow regulation, and inflammatory responses.
  • Evaluation of tissue injury and susceptibility to inflammatory conditions and septic shock.

    • Main Results:

    • NO from nNOS acts as a major inhibitory neurotransmitter.
    • NO from eNOS is crucial for physiological blood flow regulation.
    • NO from iNOS contributes to hypotension in severe inflammation.
    • NOS-deficient mice exhibit distinct phenotypes: nNOS-deficient mice show gastric issues, eNOS-deficient mice have hypotension, and iNOS-deficient mice display altered inflammatory and septic shock responses.

    Conclusions:

    • Knockout mouse models effectively distinguish the specific roles of NO from each NOS isoform.
    • Life-long NOS deficiency leads to significant and distinct physiological alterations.
    • These findings highlight the complex and isoform-specific contributions of nitric oxide to health and disease.