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

L-158,809 and (D-Ala(7))-angiotensin I/II (1-7) decrease PAI-1 release from human umbilical vein endothelial cells.

Masaya Yoshida1, Yasuhisa Naito, Tetsumei Urano

  • 1Department of Physiology, School of Medicine, Hamamatsu University, 1-20-1 Handa-yama, Hamamatsu, Shizuoka-ken 431-3192, Japan.

Thrombosis Research
|July 2, 2002
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

Active dependency formation and ambiguity resolution in real-time sentence processing.

Memory & cognition·2026
Same author

Noncovalent Synthesis of Amphiphilic Block Copolymers Through Host-Guest Interactions.

Chemistry, an Asian journal·2026
Same author

Real-time resolution of VP ellipsis ambiguity and processing depth.

Psychonomic bulletin & review·2026
Same author

Structural phases in Ca<sup>2+</sup>-triggered alginate assembly and gelation: circular dichroism-guided multimodal analysis.

Soft matter·2026
Same author

Microthrombi growth in ADAMTS13 deficiency exacerbates inflammatory bowel disease via mucosal and endothelial dysfunction.

Journal of thrombosis and haemostasis : JTH·2025
Same author

Effects of room temperature on home morning, evening, and sleep blood pressure: the Shizuoka study.

Journal of hypertension·2025

Angiotensin II (Ang II) increases plasminogen activator inhibitor-1 (PAI-1) release, while angiotensin-(1-7) (Ang-(1-7)) decreases it. Specific antagonists L-158,809 and (D-Ala(7))-angiotensin I/III (1-7) show potential as profibrinolytic drugs by modulating PAI-1 release.

Area of Science:

  • Endothelial cell biology
  • Cardiovascular physiology
  • Fibrinolysis regulation

Background:

  • The endothelium releases plasminogen activator inhibitor-1 (PAI-1), crucial for fibrinolysis.
  • Angiotensin II (Ang II) is known to upregulate endothelial PAI-1 expression.

Purpose of the Study:

  • To investigate the impact of various angiotensin-related substances on PAI-1 release from human umbilical vein endothelial cells (HUVECs).
  • To evaluate the potential of specific receptor antagonists in modulating PAI-1 and tissue plasminogen activator (t-PA) release.

Main Methods:

  • Treatment of HUVECs with Ang II, angiotensin-(1-7) (Ang-(1-7)), Angiotensin Type 1 (AT1) receptor antagonist L-158,809 (L-1), Ang-(1-7) receptor antagonist (D-Ala(7))-angiotensin I/II (1-7) (D-Ala), and Angiotensin Type 2 (AT2) antagonist PD123,319 (PD).

Related Experiment Videos

  • Measurement of PAI-1 and t-PA release in response to these treatments and their combinations.

    • Main Results:

    • Ang II stimulated PAI-1 and t-PA release, whereas Ang-(1-7) inhibited it.
    • L-1 and D-Ala decreased PAI-1 and t-PA release; PD had no effect.
    • D-Ala demonstrated a dose-dependent decrease in PAI-1 release when combined with Ang II or Ang-(1-7).

    Conclusions:

    • L-158,809 and (D-Ala(7))-angiotensin I/III (1-7) exhibit profibrinolytic properties by influencing PAI-1 release.
    • These agents may hold therapeutic potential in conditions involving dysregulated fibrinolysis.