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Hydrogen sulfide (H 2 S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder
Author(s) -
Patacchini Riccardo,
Santicioli Paolo,
Giuliani Sandro,
Maggi Carlo Alberto
Publication year - 2004
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705764
Subject(s) - capsaicin , tachyphylaxis , tachykinin receptor , chemistry , tetrodotoxin , receptor , endocrinology , substance p , medicine , neurokinin a , capsazepine , pharmacology , trpv1 , neuropeptide , biology , biochemistry , transient receptor potential channel
In the rat isolated urinary bladder, NaHS (30 μ M –3 m M ) and capsaicin (10 n M –3 μ M ) produced concentration‐dependent contractile responses (pEC 50 =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 μ M 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 NK 1 (GR 82334; 10 μ M ) and NK 2 (nepadutant; 0.3 μ M ) receptor‐selective antagonists. Tetrodotoxin (1 μ M ) only partially reduced the response to NaHS. These results provide pharmacological evidence that H 2 S stimulates capsaicin‐sensitive primary afferent nerve terminals, from which tachykinins are released to produce the observed contraction by activating NK 1 and NK 2 receptors. While the molecular site of action of H 2 S remains to be investigated, our discovery may have important physiological significance since H 2 S 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