Related Experiment Video

Updated: Sep 11, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 26, 2009

Mepyramine inhibits platelet activating factor-induced rabbit platelet aggregation: role of intracellular histamine

S Zeng1, Z G Guo

  • 1Laboratory of Molecular Pharmacology, Hunan Medical University, Changsha, China.

Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica
|March 1, 1997
PubMed
Abstract

Insights

Platelet activating factor (PAF) triggers platelet activation through intracellular histamine (HA) synthesis and release. This process involves thromboxane B2 generation and calcium ion elevation, inhibited by H1 receptor antagonists.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hematology

Background:

  • Platelet activation is a complex process involving various signaling pathways.
  • Platelet activating factor (PAF) is a potent lipid mediator that induces platelet aggregation and degranulation.
  • The role of intracellular histamine in PAF-induced platelet activation requires further elucidation.

Purpose of the Study:

  • To investigate the potential involvement of intracellular histamine (HA) in platelet activation induced by platelet activating factor (PAF).
  • To determine the effect of H1 and H2 receptor antagonists on PAF-induced platelet responses.

Main Methods:

  • Utilized washed rabbit platelets to assess the inhibitory effects of mepyramine (Mep), an H1 receptor antagonist, on PAF-induced platelet aggregation.
  • Quantified thromboxane B2 (TXB2) generation using radioimmunoassay.
  • Measured intracellular calcium ([Ca2+]i) concentration with the Fura-2 fluorescence indicator.

Main Results:

  • Mepyramine demonstrated a concentration-dependent inhibition of PAF-induced platelet aggregation, with an IC50 of 162 mumol.L-1.
  • Cimetidine, an H2 receptor antagonist, showed no significant effect on PAF-induced platelet aggregation.
  • Preincubation with mepyramine inhibited PAF-induced TXB2 generation and [Ca2+]i elevation.

Conclusions:

  • PAF-induced platelet activation is linked to intracellular histamine synthesis and release.
  • This process shares a common pathway with thromboxane B2 generation and intracellular calcium ([Ca2+]i) increase.
  • H1 receptor antagonism effectively inhibits PAF-induced platelet activation, suggesting a role for intracellular histamine.

More Related Videos

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry08:04

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...