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

Decrease in ambient [Cl-] stimulates nitric oxide release from cultured rat mesangial cells

H Tsukahara1, Y Krivenko, L C Moore

  • 1Department of Medicine, Health Sciences Center, State University of New York, Stony Brook 11794-8152.

The American Journal of Physiology
|July 1, 1994
PubMed
Summary
This summary is machine-generated.

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

Gold as a Filling Material.

The Dental register·2021
Same author

Heparanase in Acute Kidney Injury.

Advances in experimental medicine and biology·2020
Same author

Birth order and paediatric allergic disease: A nationwide longitudinal survey.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2018
Same author

Therapeutic Restoration of Endothelial Glycocalyx in Sepsis.

The Journal of pharmacology and experimental therapeutics·2017
Same author

Stress-Induced Premature Senescence of Endothelial and Endothelial Progenitor Cells.

Advances in pharmacology (San Diego, Calif.)·2016
Same author

Nitrite/Nitrate in Nasal Lavage Fluid Reflects Nasal Symptoms After a Single Nasal Allergen Provocation in Patients With Seasonal Allergic Rhinitis.

Journal of investigational allergology & clinical immunology·2016
Same journal

Blood coagulation in fish.

The American journal of physiology·2011
Same journal

Renal tubular reabsorption, metabolic utilization and isomeric fractionation of lactic acid in the dog.

The American journal of physiology·2010
Same journal

The inactivation of placental toxin by human serum.

The American journal of physiology·2010
Same journal

Adrenal function following ovariectomy in the rat.

The American journal of physiology·2010
Same journal

Capillary permeability; perfusion of frog and guinea pig hind limbs.

The American journal of physiology·2010
Same journal

Evaluation of protective measures against sunburn.

The American journal of physiology·2010
See all related articles

Extraglomerular mesangial cells (MC) respond to changes in extracellular chloride levels by releasing nitric oxide (NO). This chloride-mediated NO release from MC may play a role in tubuloglomerular feedback (TGF) signal transmission.

Area of Science:

  • Nephrology
  • Cell Physiology
  • Molecular Biology

Background:

  • The juxtaglomerular apparatus (JGA) is crucial for regulating kidney function.
  • Extraglomerular mesangial cells (MC) within the JGA are hypothesized to modulate tubuloglomerular feedback (TGF).
  • Ionic fluctuations in the JGA interstitium are thought to influence MC function and TGF signaling.

Purpose of the Study:

  • To investigate the effects of altered extracellular ion concentrations on MC.
  • To determine if MC respond to changes in sodium ([Na+]) and chloride ([Cl-]) levels.
  • To explore the impact of MC activation on nitric oxide (NO) production.

Main Methods:

  • Cultured rat MC were utilized for experiments.
  • Cytosolic calcium concentration ([Ca2+]i) was measured in response to ion changes.

Related Experiment Videos

  • Amperometric NO sensors were employed to detect NO release.
  • Specific inhibitors (dexamethasone, indomethacin) were used to probe signaling pathways.

    • Main Results:

    • Reduced extracellular [Na+] and [Cl-] induced a concentration-dependent increase in [Ca2+]i in MC.
    • MC exhibited higher sensitivity to decreases in [Cl-] compared to [Na+].
    • A decrease in extracellular [Cl-] stimulated Ca2+/calmodulin-dependent NO release from MC.
    • NO release was mediated by constitutive NO synthase and potentially regulated by cyclooxygenase metabolites.

    Conclusions:

    • MC are sensitive to modest changes in extracellular chloride concentrations.
    • Chloride-induced NO release from MC offers a potential mechanism for TGF signal transmission.
    • This finding elucidates a novel role for MC in renal autoregulation via NO signaling.