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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Related Experiment Video

Updated: Jun 7, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Endothelium-derived Relaxing Factor Inhibits Shear Stress-induced Platelet Aggregation.

W Durante1, A I Schafer, J K Hrbolich

  • 1Houston VA Medical Center, Baylor College of Medicine, and Rice University, Houston, TX, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Platelets
|November 4, 2010
PubMed
Summary
This summary is machine-generated.

Endothelium-derived relaxing factor (EDRF) and nitric oxide (NO) compounds inhibit shear stress-induced platelet aggregation. This suggests that intraplatelet cyclic guanosine 3

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Last Updated: Jun 7, 2026

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The Assembly and Application of 'Shear Rings': A Novel Endothelial Model for Orbital, Unidirectional and Periodic Fluid Flow and Shear Stress
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Electrophysiological Recordings of Single-cell Ion Currents Under Well-defined Shear Stress

Published on: August 2, 2019

Area of Science:

  • Cardiovascular Physiology
  • Hematology
  • Biochemistry

Background:

  • Platelet aggregation is crucial in hemostasis and thrombosis.
  • Arterial wall shear stress is a significant physiological factor influencing platelet behavior.
  • Endothelium-derived relaxing factor (EDRF), identified as nitric oxide (NO), plays a role in vascular homeostasis.

Purpose of the Study:

  • To investigate the effect of EDRF and related compounds on platelet aggregation under varying shear stress conditions.
  • To explore the role of cyclic guanosine 3',5'-monophosphate (cGMP) in mediating the inhibitory effects on shear-induced platelet aggregation.

Main Methods:

  • Platelet aggregation was measured using a cone-plate viscometer under shear stresses ranging from 30-120 dyne/cm(2).
  • Platelets were pre-treated with S-nitrosothiol compounds, nitric oxide (NO), SIN-1, and non-hydrolyzable cGMP analogues.
  • Pharmacological agents (methylene blue, M&B 22 984) were used to manipulate NO and cGMP levels.

Main Results:

  • Shear stress markedly induced platelet aggregation in plasma and washed platelets.
  • Pre-treatment with EDRF-related compounds (S-nitroso-N-acetylcysteine, S-nitrosocysteine, NO, SIN-1) significantly reduced shear stress-induced platelet aggregation.
  • Non-hydrolyzable cGMP analogues also inhibited aggregation, and alterations in intraplatelet cGMP levels correlated with the degree of inhibition.

Conclusions:

  • EDRF and related compounds effectively inhibit platelet aggregation triggered by arterial wall shear stress.
  • Intraplatelet cGMP signaling is a key mechanism regulating the anti-aggregatory effects of EDRF/NO in response to shear stress.
  • These findings highlight a crucial physiological pathway for controlling platelet activation in response to hemodynamic forces.