Hydrogen sulfide (H2S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder

In the rat isolated urinary bladder, NaHS (30 μM–3 mM) and capsaicin (10 nM–3 μM) produced concentration‐dependent contractile responses (pEC50=3.5±0.02 and 7.1±0.02, respectively) undergoing dramatic tachyphylaxis. In preparations in which sensory nerves were rendered desensitized (defunctionalized...

Full description

Saved in:
Bibliographic Details
Published in:British journal of pharmacology 2004-05, Vol.142 (1), p.31-34
Main Authors: Patacchini, Riccardo, Santicioli, Paolo, Giuliani, Sandro, Maggi, Carlo Alberto
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
capsaicin
Capsaicin - pharmacology
Dose-Response Relationship, Drug
Hydrogen sulfide (H2S)
Hydrogen Sulfide - metabolism
Hydrogen Sulfide - pharmacology
Male
Medical sciences
Neurons, Afferent - drug effects
Neurons, Afferent - physiology
Pharmacology. Drug treatments
Rats
Rats, Wistar
sensory nerves
Special Reports
tachykinin receptors
tachykinins
Urinary Bladder - drug effects
Urinary Bladder - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In the rat isolated urinary bladder, NaHS (30 μM–3 mM) and capsaicin (10 nM–3 μM) produced concentration‐dependent contractile responses (pEC50=3.5±0.02 and 7.1±0.02, respectively) undergoing dramatic tachyphylaxis. In preparations in which sensory nerves were rendered desensitized (defunctionalized) by high‐capsaicin (10 μM for 15 min) pretreatment, neither capsaicin itself nor NaHS produced any motor effect. NaHS‐induced contractile effects were totally prevented by the simultaneous incubation with tachykinin NK1 (GR 82334; 10 μM) and NK2 (nepadutant; 0.3 μM) receptor‐selective antagonists. Tetrodotoxin (1 μM) only partially reduced the response to NaHS. These results provide pharmacological evidence that H2S stimulates capsaicin‐sensitive primary afferent nerve terminals, from which tachykinins are released to produce the observed contraction by activating NK1 and NK2 receptors. While the molecular site of action of H2S remains to be investigated, our discovery may have important physiological significance since H2S concentrations capable of stimulating sensory nerves overlap those occurring in mammalian tissues under normal conditions. British Journal of Pharmacology (2004) 142, 31–34. doi:10.1038/sj.bjp.0705764
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0705764