The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation

G. Pozsgai, Zsófia Hajna, Teréz Bagoly, Melinda Boros, Ágnes Kemény, Serena Materazzi, Romina Nassini, Z. Helyes, J. Szolcsányi, E. Pintér

Research output: Contribution to journalArticle

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Abstract

Activation of transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) channels on capsaicin-sensitive sensory neurons causes release of inflammatory neuropeptides, including calcitonin gene-related peptide (CGRP). We investigated whether the hydrogen sulphide (H2S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H2S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Allylisothiocyanate (AITC) or the H2S donor sodium hydrogen sulphide (NaHS) were used as stimuli and CGRP release of the rat tracheae was measured by radioimmunoassay. AITC or NaHS were applied to the ears of Balb/c, C57BL/6, TRPA1 and TRPV1 receptor gene knockout mice and blood flow was detected by laser Doppler imaging. Both AITC and NaHS increased CGRP release from isolated rat tracheae, and both responses were inhibited by the TRPA1 antagonist, HC-030031, but was not affected by the TRPV1 receptor blocker, BCTC. Application of AITC or NaHS increased the cutaneous blood flow in the mouse ears. Similarly to the effect of AITC, the vasodilatory response to NaHS was reduced by HC-030031 or in TRPA1 deleted mice. In contrast, genetic deletion of TRPV1 did not affect the increase in the ear blood flow evoked by AITC or NaHS. We conclude that H2S activates TRPA1 receptors causing CGRP release from sensory nerves of rat tracheae, as well as inducing cutaneous vasodilatation in the mouse ear. TRPV1 receptors were not involved in these processes. Our results highlight that TRPA1 receptor activation should be considered as a potential mechanism of vasoactive effects of H2S.

Original languageEnglish
Pages (from-to)56-64
Number of pages9
JournalEuropean Journal of Pharmacology
Volume689
Issue number1-3
DOIs
Publication statusPublished - Aug 15 2012

Fingerprint

Ankyrins
Hydrogen Sulfide
Calcitonin Gene-Related Peptide
Vasodilation
Ear
Trachea
Sensory Receptor Cells
Calcitonin Gene-Related Peptide Receptors
Skin
Gene Knockout Techniques
Capsaicin
Microcirculation
Neuropeptides
Knockout Mice
Radioimmunoassay
sodium bisulfide
Lasers
vanilloid receptor subtype 1

Keywords

  • CGRP
  • HC-030031
  • Hydrogen sulphide
  • Laser Doppler imaging
  • TRPA1 receptor
  • Vasodilatation

ASJC Scopus subject areas

  • Pharmacology

Cite this

The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation. / Pozsgai, G.; Hajna, Zsófia; Bagoly, Teréz; Boros, Melinda; Kemény, Ágnes; Materazzi, Serena; Nassini, Romina; Helyes, Z.; Szolcsányi, J.; Pintér, E.

In: European Journal of Pharmacology, Vol. 689, No. 1-3, 15.08.2012, p. 56-64.

Research output: Contribution to journalArticle

Pozsgai, G. ; Hajna, Zsófia ; Bagoly, Teréz ; Boros, Melinda ; Kemény, Ágnes ; Materazzi, Serena ; Nassini, Romina ; Helyes, Z. ; Szolcsányi, J. ; Pintér, E. / The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation. In: European Journal of Pharmacology. 2012 ; Vol. 689, No. 1-3. pp. 56-64.
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