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 of bradykinin-induced glomerular contraction in diabetic rat: a new cellular interpretation

M Ouardani1, P Travo, J Rakotoarivony

  • 1INSERM U 388, Institut Louis Bugnard, CHU Rangueil, Toulouse/France.

European Journal of Cell Biology
|July 1, 1997
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

A 3D reconstruction of pancreas development in the human embryos during embryonic period (Carnegie stages 15-23).

Surgical and radiologic anatomy : SRA·2009
Same author

Contribution to the 3D computer assisted reconstruction of pancreatic buds in the rat embryos.

Surgical and radiologic anatomy : SRA·2008
Same author

Diagnosis and differentiation of Mycoplasma hyopneumoniae and Mycoplasma hyorhinis infections in pigs by PCR amplification of the p36 and p46 genes.

Journal of clinical microbiology·2000
Same author

Human 76p: A new member of the gamma-tubulin-associated protein family.

The Journal of cell biology·1999
Same author

Multiplex PCR for detection and typing of porcine circoviruses.

Journal of clinical microbiology·1999
Same author

An hypothesis for the interpretation of the contractile response of vascular smooth muscle at the cellular level.

Cell biology and toxicology·1996

Diabetic rats show reduced kidney glomeruli and mesangial cell contraction due to bradykinin (BK). This impairment involves decreased calcium signaling and protein kinase C (PKC) pathway alterations, suggesting early diabetic kidney dysfunction.

Area of Science:

  • Nephrology
  • Diabetology
  • Cell Biology

Background:

  • Diabetes mellitus is associated with early glomerular hemodynamic changes.
  • The contractile function of glomerular and mesangial cells plays a role in regulating renal hemodynamics.
  • Understanding cellular mechanisms underlying these changes is crucial for early intervention.

Purpose of the Study:

  • To investigate the contractile response of glomeruli and mesangial cells (MC) to bradykinin (BK) in early diabetes.
  • To explore the role of calcium signaling and protein kinase C (PKC) pathways in diabetic mesangial cell dysfunction.
  • To assess the potential therapeutic effect of insulin on diabetic mesangial cell contractility.

Main Methods:

  • Isolated glomeruli and mesangial cells from streptozotocin-induced diabetic rats and control rats were used.

Related Experiment Videos

  • Contractile responses were measured by changes in cell surface area upon BK stimulation.
  • Glomerular calcium uptake and intracellular calcium mobilization in MC were assessed.
  • PKC inhibitors were used to probe the involvement of PKC signaling.
  • Insulin's effect on cell contractility was evaluated.

    • Main Results:

    • Diabetic glomeruli and MC exhibited significantly reduced contractile responses to BK compared to normal rats.
    • This reduction was linked to decreased glomerular calcium uptake and MC intracellular calcium mobilization.
    • PKC inhibition mimicked the reduced contractility in normal cells, suggesting PKC pathway involvement in diabetes.
    • Insulin treatment partially restored the contractile function of diabetic MC, particularly affecting the proportion of contractile cells.
    • Contraction index (CI) changes in cultured cells mirrored those in intact glomeruli.

    Conclusions:

    • Early diabetes in rats is characterized by impaired glomerular and mesangial cell contractility.
    • A compromised protein kinase C (PKC) pathway and altered calcium handling contribute to this dysfunction.
    • Insulin shows potential in ameliorating these early diabetic kidney contractile abnormalities.
    • The study highlights the kallikrein-kinin system's potential role in early diabetic nephropathy.