Back
Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary
ROLE OF TRANSIENT RECEPTOR POTENTIAL ANKYRIN 1 (TRPA1) RECEPTORS IN HYDROGEN SULPHIDE-EVOKED CALCITONIN GENE-RELATED PEPTIDE (CGRP) RELEASE FROM ISOLATED RAT TRACHEAE
Abstract number: P71
Pozsgai1 G., Bagoly1 T., Hajna1 Zs., Boros1 M., Helyes1 Zs., Szolcsanyi1 J., Pinter1 E.
Aims:
TRPA1 receptors are present on peptidergic sensory neurons. TRPA1 receptors are non-selective cation channels activated by airway irritants, nucleophilic reactive compounds, reactive oxygen species and some plant derived pungent agents (e.g. allylisothiocyanate, AITC). Activation of TRPA1 receptors results in release of sensory neuropeptides (e.g. calcitonin gene-related peptide, CGRP) that induce neurogenic inflammation. Hydrogen sulphide (H2S) is an endogenous gaseous mediator influencing the cardiovascular system, inflammation, etc. It has been shown recently that H2S activates peptidergic sensory neurons of the airways and urinary bladder. In the present study we investigated the effect of H2S on CGRP release from sensory nerve fibres of isolated rat tracheae. Effect of H2S was compared to that of TRPA1 receptor agonist AITC.
Methods:
Isolated rat tracheae were placed in organ baths and perfused with oxygenated Krebs-Henseleit solution at 37°C. AITC, H2S donor sodium hydrogen sulphide (NaHS) or electrical field stimulation (40 V. 0.1 ms, 10 Hz, 120 s, EFS) were used to evoke CGRP release from sensory nerves. CGRP concentration of the perfusing solution was measured by radioimmunoassay. Selective TRPA1 receptor antagonist HC030031 was used to examine involvement of TRPA1 receptors in CGRP release.
Results:
Both AITC and NaHS induced dose dependent CGRP release from isolated rat tracheae. EC50 values were 56.25 mmol/l and 0.96 mmol/l, respectively. TRPA1 receptor antagonist HC030031 significantly inhibited both AITC and NaHS-evoked CGRP release. EFS-induced CGRP release was not influenced by HC030031. Administration of NaHS significantly increased EFS-induced CGRP release.
Conclusion:
H2S has been shown to exert its effect via modulation of various ion channels, enzymes, transcription factors and protein S-sulfhydration. Here we provide evidence that gaseous transmitter H2S is a putative endogenous agonist of TRPA1 receptors and may contribute to pathologic conditions involving neurogenic inflammation.
Support:
OTKA K-81984 and Baross Gábor Programme
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :P71