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

Potassium uptake and release by human blood platelets

J S Wiley, J Kuchibhotla, C C Shaller

    Blood
    |August 1, 1976
    PubMed
    Summary

    Thrombin induces potassium (K+) loss from human platelets, primarily from alpha-granules, not cell lysis. This finding helps understand platelet activation and drug effects on K+ release.

    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

    Shear stress modulates endothelial KLF2 through activation of P2X4.

    Purinergic signalling·2015
    Same author

    The human P2X7 receptor and its role in innate immunity.

    Tissue antigens·2011
    Same author

    Recent developments in murine typhus fever control.

    American journal of public health and the nation's health·2010
    Same author

    Evidence for associations between the purinergic receptor P2X(7) (P2RX7) and toxoplasmosis.

    Genes and immunity·2010
    Same author

    Targeting ErbB2 and ErbB3 with a bispecific single-chain Fv enhances targeting selectivity and induces a therapeutic effect in vitro.

    British journal of cancer·2008
    Same author

    The genetic control of susceptibility to Mycobacterium tuberculosis.

    Novartis Foundation symposium·2007

    Area of Science:

    • Hematology
    • Cell Biology
    • Biochemistry

    Background:

    • Thrombin is known to decrease potassium (K+) content in human platelets.
    • The subcellular source of this K+ loss remains unidentified.

    Purpose of the Study:

    • To investigate the subcellular origin of K+ released from human platelets upon stimulation by aggregating agents.
    • To determine the role of alpha-granules in thrombin-induced K+ release.

    Main Methods:

    • Human platelets were labeled with 42K+ and separated by gel filtration.
    • Platelets were treated with various aggregating agents (epinephrine, ADP, thrombin).
    • Release of K+, serotonin, beta-glucuronidase, and lactic dehydrogenase was measured.

    Main Results:

    • Thrombin induced a significant K+ loss (up to 30%) and released beta-glucuronidase, an alpha-granule enzyme.
    • Epinephrine and ADP caused minimal K+ loss without beta-glucuronidase release.
    • A linear correlation was observed between K+ and beta-glucuronidase release induced by thrombin.
    • Aspirin inhibited thrombin-induced serotonin release but not K+ or beta-glucuronidase release when applied in vitro.

    Conclusions:

    • Thrombin-induced K+ loss in human platelets originates mainly from alpha-granules.
    • Alpha-granules contain a substantial pool of readily exchangeable K+.
    • Oral aspirin administration affects thrombin-induced release of serotonin, beta-glucuronidase, and K+.

    Related Experiment Videos