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

Redox-dependent coronary metabolic dilation.

Shu-ichi Saitoh1, Takahiko Kiyooka, Petra Rocic

  • 1Department of Integrative Medical Sciences, Northeastern Ohio University College of Medicine, 4209 State Rte. 44, Rootstown, OH 44272-0095, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|October 30, 2007
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 microstructurally motivated framework to study autoregulation in the coronary circulation.

The Journal of physiology·2026
Same author

Association of reduced Cu,Zn-superoxide dismutase with coronary microvascular dysfunction-An observational study of oxidative stress markers.

International journal of cardiology. Heart & vasculature·2026
Same author

Functional consequences of diminished myocardial oxygen delivery per beat in experimental heart failure.

Basic research in cardiology·2026
Same author

Analyzing the role of ATP-dependent potassium channels in the regulation of coronary metabolic vasodilation during exercise.

Basic research in cardiology·2026
Same author

Controlled Attenuation Parameter and Gallstone Disease Risk: A Retrospective Cohort Study with Mediation Analysis and Longitudinal Trajectory Modeling, Emphasizing Gender-Specific Effects.

Clinical epidemiology·2026
Same author

Switching from Conventional Fibrates to Pemafibrate Improves Lipid Profiles, Liver Enzymes, Renal Function, and Fibrosis Markers in Dyslipidemic Patients with MASLD: A Multicenter Real-World Study.

Journal of atherosclerosis and thrombosis·2026
Same journal

Interplay of Oxidative Stress and Inflammatory Mechanisms in Doxorubicin-induced Cardiomyopathy.

American journal of physiology. Heart and circulatory physiology·2026
Same journal

Impact of moderate isocapnic hyperthermia on dynamic cerebral autoregulation and its directional sensitivity.

American journal of physiology. Heart and circulatory physiology·2026
Same journal

Repetitive Pressure Overload; Species Disparities, Mechanisms and Translational Relevance.

American journal of physiology. Heart and circulatory physiology·2026
Same journal

SIRT2-mediated regulation of glycolytic flux: Another brick in the wall of Gary Lopaschuk's legacy in cardiac metabolism.

American journal of physiology. Heart and circulatory physiology·2026
Same journal

Tailored anesthesia protocols for echo-based HFpEF phenotyping in C57BL6/N mice.

American journal of physiology. Heart and circulatory physiology·2026
Same journal

Desmoglein-2 Deficiency Drives Mitochondrial Morphological Remodeling in Cardiomyocytes.

American journal of physiology. Heart and circulatory physiology·2026
See all related articles

Hydrogen peroxide (H2O2) causes coronary vasodilation by oxidizing intracellular thiols, activating p38 MAP kinase. This redox mechanism links myocardial oxygen consumption to coronary blood flow.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Redox Signaling
  • Molecular Cardiology

Background:

  • Hydrogen peroxide (H2O2) is a key mediator of coronary metabolic vasodilation.
  • The precise molecular mechanisms underlying H2O2-induced vasodilation, particularly its redox-dependent nature, require further elucidation.
  • Thiol oxidation is a potential pathway for H2O2 signaling in cardiovascular tissues.

Purpose of the Study:

  • To investigate the role of thiol oxidation in mediating coronary vasodilation induced by H2O2 and cardiac myocyte-released factors.
  • To identify the cellular location of thiol oxidation during vasodilation.
  • To determine if the p38 mitogen-activated protein (MAP) kinase pathway is involved in this redox-mediated dilation.

Main Methods:

  • Isolated coronary arterioles were exposed to conditioned buffer from paced cardiac myocytes and authentic H2O2.

Related Experiment Videos

  • Dilation responses were assessed with and without thiol-reducing agents (dithiothreitol and N-acetyl-L-cysteine).
  • Intracellular vs. extracellular thiol oxidation was localized using fluorescent probes; p38 MAP kinase involvement was tested using SB-203580 and Western blotting for phospho-p38.

    • Main Results:

    • Both H2O2 and myocyte-conditioned buffer induced significant vasodilation.
    • Dilation to both stimuli was attenuated by thiol-reducing agents, indicating a role for thiol oxidation.
    • Oxidation predominantly occurred in intracellular thiols, and p38 MAP kinase inhibition significantly reduced vasodilation, with H2O2 activating p38.

    Conclusions:

    • Coronary metabolic vasodilation, mediated by H2O2, involves the oxidation of intracellular thiols.
    • The p38 MAP kinase pathway is a critical downstream effector in this redox-dependent signaling cascade.
    • These findings reveal a novel redox-based mechanism coupling myocardial metabolism to coronary blood flow.