Effects of inflammatory neuropeptides on the arachidonate cascade of platelets

Árpád Gecse, Béla Kis, Zsófia Mezei, G. Telegdy

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: During neurogenic inflammation, neuropeptides (substance P, SP, calcitonin gene-related peptide, CGRP, and neurokinin A) are released from nerve endings, and these peptides initiate inflammatory reactions in the microcirculation. Platelets are one of the most important elements of the microcirculation. Methods: Our in vitro experiments were carried out to determine the effects of inflammatory neuropeptides (SP, and CGRP) on the arachidonate cascade of isolated rat platelets. Cells were labeled with 1-14C-arachidonic acid, then the eicosanoids were separated with overpressure thin-layer chromatography or high-performance liquid chromatography and were quantitatively determined with a liquid scintillation analyzer. Results: SP (10-9 and 10-8 mol/l) significantly increased the activity of the arachidonate cascade. The lipoxygenase pathway was significantly stimulated by SP (10-11, 10-9 and 10-8 mol/l), while the cyclooxygenase system was inhibited by 10-12 mol/l, and stimulated by 10-9 mol/l SP. The dose-response curve of TxA2 to SP exhibited a similar pattern to that detected for the cyclooxygenase pathway. Among the vasodilator cyclooxygenase metabolites, only the synthesis of PGE2 was significantly elevated by SP (10-9 mol/l). CGRP either in low (10-12-10-11 mol/l) or in high concentrations (10-6 mol/l) activated the cyclooxygenase pathway, while it had no effect on the lipoxygenase pathway. CGRP (8-37), a specific CGRP1 receptor antagonist, inhibited the effects of CGRP. Conclusions: Our data suggest that the arachidonate metabolites of platelets may play a role in the process of neurogenic inflammation.

Original languageEnglish
Pages (from-to)166-170
Number of pages5
JournalInternational Archives of Allergy and Immunology
Volume118
Issue number2-4
Publication statusPublished - 1999

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Prostaglandin-Endoperoxide Synthases
Neuropeptides
Blood Platelets
Neurogenic Inflammation
Lipoxygenase
Microcirculation
Neurokinin A
Nerve Endings
Eicosanoids
Calcitonin Gene-Related Peptide
Substance P
Thin Layer Chromatography
Vasodilator Agents
Dinoprostone
Arachidonic Acid
High Pressure Liquid Chromatography
Peptides

Keywords

  • 12-HETE
  • CGRP
  • Platelets
  • Prostaglandins
  • Substance P
  • Thromboxane

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Effects of inflammatory neuropeptides on the arachidonate cascade of platelets. / Gecse, Árpád; Kis, Béla; Mezei, Zsófia; Telegdy, G.

In: International Archives of Allergy and Immunology, Vol. 118, No. 2-4, 1999, p. 166-170.

Research output: Contribution to journalArticle

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abstract = "Background: During neurogenic inflammation, neuropeptides (substance P, SP, calcitonin gene-related peptide, CGRP, and neurokinin A) are released from nerve endings, and these peptides initiate inflammatory reactions in the microcirculation. Platelets are one of the most important elements of the microcirculation. Methods: Our in vitro experiments were carried out to determine the effects of inflammatory neuropeptides (SP, and CGRP) on the arachidonate cascade of isolated rat platelets. Cells were labeled with 1-14C-arachidonic acid, then the eicosanoids were separated with overpressure thin-layer chromatography or high-performance liquid chromatography and were quantitatively determined with a liquid scintillation analyzer. Results: SP (10-9 and 10-8 mol/l) significantly increased the activity of the arachidonate cascade. The lipoxygenase pathway was significantly stimulated by SP (10-11, 10-9 and 10-8 mol/l), while the cyclooxygenase system was inhibited by 10-12 mol/l, and stimulated by 10-9 mol/l SP. The dose-response curve of TxA2 to SP exhibited a similar pattern to that detected for the cyclooxygenase pathway. Among the vasodilator cyclooxygenase metabolites, only the synthesis of PGE2 was significantly elevated by SP (10-9 mol/l). CGRP either in low (10-12-10-11 mol/l) or in high concentrations (10-6 mol/l) activated the cyclooxygenase pathway, while it had no effect on the lipoxygenase pathway. CGRP (8-37), a specific CGRP1 receptor antagonist, inhibited the effects of CGRP. Conclusions: Our data suggest that the arachidonate metabolites of platelets may play a role in the process of neurogenic inflammation.",
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N2 - Background: During neurogenic inflammation, neuropeptides (substance P, SP, calcitonin gene-related peptide, CGRP, and neurokinin A) are released from nerve endings, and these peptides initiate inflammatory reactions in the microcirculation. Platelets are one of the most important elements of the microcirculation. Methods: Our in vitro experiments were carried out to determine the effects of inflammatory neuropeptides (SP, and CGRP) on the arachidonate cascade of isolated rat platelets. Cells were labeled with 1-14C-arachidonic acid, then the eicosanoids were separated with overpressure thin-layer chromatography or high-performance liquid chromatography and were quantitatively determined with a liquid scintillation analyzer. Results: SP (10-9 and 10-8 mol/l) significantly increased the activity of the arachidonate cascade. The lipoxygenase pathway was significantly stimulated by SP (10-11, 10-9 and 10-8 mol/l), while the cyclooxygenase system was inhibited by 10-12 mol/l, and stimulated by 10-9 mol/l SP. The dose-response curve of TxA2 to SP exhibited a similar pattern to that detected for the cyclooxygenase pathway. Among the vasodilator cyclooxygenase metabolites, only the synthesis of PGE2 was significantly elevated by SP (10-9 mol/l). CGRP either in low (10-12-10-11 mol/l) or in high concentrations (10-6 mol/l) activated the cyclooxygenase pathway, while it had no effect on the lipoxygenase pathway. CGRP (8-37), a specific CGRP1 receptor antagonist, inhibited the effects of CGRP. Conclusions: Our data suggest that the arachidonate metabolites of platelets may play a role in the process of neurogenic inflammation.

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