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

Cerebral artery sarcoplasmic reticulum Ca(2+) stores and contractility: changes with development.

W Long1, L Zhang, L D Longo

  • 1Center for Perinatal Biology, Departments of Physiology/Pharmacology and Obstetrics and Gynecology, School of Medicine, Loma Linda University, Loma Linda, California 92350, USA.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|August 24, 2000
PubMed
Summary

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

Antenatal maternal hypoxic stress: adaptations of the placental renin-angiotensin system in the mouse.

Placenta·2010
Same author

Placental gene expression in a rat 'model' of placental insufficiency.

Placenta·2010
Same author

Placental gene expression responses to maternal protein restriction in the mouse.

Placenta·2009
Same author

Upregulation of eNOS in pregnant ovine uterine arteries by chronic hypoxia.

American journal of physiology. Heart and circulatory physiology·2001
Same author

Cerebral artery K(ATP)- and K(Ca)-channel activity and contractility: changes with development.

American journal of physiology. Regulatory, integrative and comparative physiology·2000
Same author

Dual role of PKC in modulating pharmacomechanical coupling in fetal and adult cerebral arteries.

American journal of physiology. Regulatory, integrative and comparative physiology·2000

Sarcoplasmic reticulum Ca(2+) stores are less critical for fetal cerebral artery contraction than adult. Norepinephrine-induced contraction in fetal arteries primarily relies on external calcium influx via L-type channels.

Area of Science:

  • Cardiovascular Physiology
  • Developmental Biology
  • Smooth Muscle Pharmacology

Background:

  • Sarcoplasmic reticulum (SR) Ca(2+) stores are crucial for regulating vascular smooth muscle contraction.
  • Developmental changes in cerebral artery function may alter the contribution of SR Ca(2+) stores to norepinephrine (NE)-induced responses.

Purpose of the Study:

  • To investigate the role of SR Ca(2+) stores in NE-induced contraction of fetal and adult sheep middle cerebral arteries (MCA).
  • To determine if developmental changes influence the reliance on SR Ca(2+) stores for cerebral artery contraction.

Main Methods:

  • Measured NE-induced tension and intracellular Ca(2+) ([Ca(2+)](i)) in fetal and adult sheep MCA.
  • Utilized thapsigargin and ryanodine to assess the contribution of SR Ca(2+) stores and ryanodine receptors.

Related Experiment Videos

  • Performed experiments in the presence and absence of extracellular Ca(2+).

    • Main Results:

    • Thapsigargin significantly reduced NE-induced responses in adult MCA but not in fetal MCA.
    • Absence of extracellular Ca(2+) markedly impaired NE-induced responses in adult MCA, with minimal effect on fetal MCA.
    • Ryanodine application mimicked NE-induced responses, which were abolished in zero extracellular Ca(2+).

    Conclusions:

    • SR Ca(2+) stores play a significantly lesser role in NE-induced contraction of fetal MCA compared to adult MCA.
    • Fetal cerebral artery contraction is predominantly mediated by Ca(2+) influx through plasma membrane L-type Ca(2+) channels.
    • The ryanodine receptor in both fetal and adult MCA appears coupled to plasma membrane channels, influencing contraction.