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Phosphoinositides and cicletanine.

P Marche1, A Girard

  • 1Department of Pharmacology, INSERM U7, CNRS UA318, Necker Hospital, Paris, France.

Drugs Under Experimental and Clinical Research
|January 1, 1988
PubMed
Summary
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Cicletanine blocks histamine-induced phosphoinositide metabolism in vascular smooth muscle cells, acting as an H1 receptor antagonist. This action may contribute to cicletanine's antihypertensive effects by modulating intracellular calcium levels.

Area of Science:

  • Pharmacology
  • Vascular Biology
  • Cell Signaling

Background:

  • Histamine H1 receptor activation increases cytosolic calcium in vascular smooth muscle cells.
  • This calcium increase is linked to inositol lipid metabolism.
  • Cicletanine exhibits characteristics of an H1 antagonist.

Purpose of the Study:

  • To investigate if cicletanine antagonizes H1 receptor-mediated phosphoinositide metabolism.
  • To elucidate the role of phosphoinositide metabolism in histamine's effects on vascular smooth muscle.

Main Methods:

  • Cultured guinea-pig aortic smooth muscle cells were used.
  • Phosphoinositide metabolism was assessed via 32P labeling of phosphatidylinositol (PI) and its derivatives.
  • Cells were treated with histamine, H1/H2 agonists, and antagonists, including cicletanine.

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Main Results:

  • Histamine and the H1 agonist 2-PEA selectively increased 32P-PI labeling.
  • This increase was inhibited by the H1 antagonist mepyramine but not the H2 antagonist cimetidine.
  • Cicletanine inhibited the 32P-PI increase with an IC50 of 10(-6) M, similar to mepyramine.

Conclusions:

  • Histamine-induced 32P-PI increase is mediated via H1 receptors.
  • Cicletanine acts as an H1 receptor antagonist in this cellular model.
  • Cicletanine's blockade of histamine-enhanced phosphoinositide turnover may contribute to its antihypertensive action.