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Related Experiment Videos

The plasminogen activator system modulates sympathetic nerve function.

Ulrich Schaefer1, Takuji Machida, Sandra Vorlova

  • 1Department of Pharmacology, Weill Medical College of Cornell University, New York, NY 10021, USA.

The Journal of Experimental Medicine
|August 31, 2006
PubMed
Summary
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Tissue plasminogen activator (t-PA) enhances norepinephrine release from sympathetic nerves, impacting cardiac function and arrhythmias. Inhibiting t-PA reduces sympathetic activity, while its absence protects against ischemia-reperfusion arrhythmias.

Area of Science:

  • Neuroscience
  • Cardiovascular Biology
  • Biochemistry

Background:

  • Sympathetic neurons release tissue plasminogen activator (t-PA).
  • The role of t-PA in modulating sympathetic nervous system activity is not fully understood.
  • Norepinephrine (NE) release is critical for sympathetic neurotransmission and cardiac function.

Purpose of the Study:

  • To investigate the role of t-PA in regulating sympathetic activity.
  • To determine if t-PA influences norepinephrine release and sympathetic nerve function.
  • To assess the impact of t-PA on cardiac arrhythmias during ischemia/reperfusion.

Main Methods:

  • Inhibition of t-PA in guinea pig vas deferens and cardiac synaptosomes.
  • Administration of recombinant t-PA (rt-PA) to cardiac synaptosomes and neuroblastoma cells.

Related Experiment Videos

  • Assessment of norepinephrine (NE) release and exocytosis.
  • Electrophysiological studies on vasa deferentia from t-PA-null and PAI-1-null mice.
  • Analysis of cardiac NE overflow and arrhythmias in t-PA-null mice during ischemia/reperfusion.

    • Main Results:

    • t-PA inhibition reduced vas deferens contraction and NE exocytosis.
    • rt-PA induced NE release in a plasmin-independent manner, potentiated by fibrinogen cleavage products.
    • t-PA-null mice showed significantly reduced NE release and hyporesponsive vasa deferentia.
    • PAI-1-null mice exhibited increased NE release and hyperresponsive vasa deferentia.
    • t-PA-null hearts displayed reduced NE overflow and fewer reperfusion arrhythmias.

    Conclusions:

    • t-PA enhances NE release from sympathetic nerves.
    • t-PA contributes to cardiac arrhythmias during ischemia/reperfusion.
    • Targeting t-PA's NE-releasing effect may offer therapeutic potential for hyperadrenergic conditions and sudden cardiac death.