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Hydrogen sulfide mediated inhibitory neurotransmission to the pig bladder neck: role of KATP channels, sensory nerves and calcium signaling.
J Urol. 2013 Aug; 190(2):746-56.JU

Abstract

PURPOSE

Because neuronal released endogenous H2S has a key role in relaxation of the bladder outflow region, we investigated the mechanisms involved in H2S dependent inhibitory neurotransmission to the pig bladder neck.

MATERIALS AND METHODS

Bladder neck strips were mounted in myographs for isometric force recording and simultaneous measurement of intracellular Ca(2+) and tension.

RESULTS

On phenylephrine contracted preparations electrical field stimulation and the H2S donor GYY4137 evoked frequency and concentration dependent relaxation, which was reduced by desensitizing capsaicin sensitive primary afferents with capsaicin, and the blockade of adenosine 5'-triphosphate dependent K(+) channels, cyclooxygenase and cyclooxygenase-1 with glibenclamide, indomethacin and SC560, respectively. Inhibition of vanilloid, transient receptor potential A1, transient receptor potential vanilloid 1, vasoactive intestinal peptide/pituitary adenylyl cyclase-activating polypeptide and calcitonin gene-related peptide receptors with capsazepine, HC030031, AMG9810, PACAP6-38 and CGRP8-37, respectively, also decreased electrical field stimulation and GYY4137 responses. H2S relaxation was not changed by guanylyl cyclase, protein kinase A, or Ca(2+) activated or voltage gated K(+) channel inhibitors. GYY4137 inhibited the contractions induced by phenylephrine and by K(+) enriched (80 mM) physiological saline solution. To a lesser extent it decreased the phenylephrine and K(+) induced increases in intracellular Ca(2+).

CONCLUSIONS

H2S produces pig bladder neck relaxation via activation of adenosine 5'-triphosphate dependent K(+) channel and by smooth muscle intracellular Ca(2+) desensitization dependent mechanisms. H2S also promotes the release of sensory neuropeptides and cyclooxygenase-1 pathway derived prostanoids from capsaicin sensitive primary afferents via transient receptor potential A1, transient receptor potential vanilloid 1 and/or related ion channel activation.

Authors+Show Affiliations

Departamento de Fisiología, Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23454157

Citation

Fernandes, Vítor S., et al. "Hydrogen Sulfide Mediated Inhibitory Neurotransmission to the Pig Bladder Neck: Role of KATP Channels, Sensory Nerves and Calcium Signaling." The Journal of Urology, vol. 190, no. 2, 2013, pp. 746-56.
Fernandes VS, Ribeiro AS, Barahona MV, et al. Hydrogen sulfide mediated inhibitory neurotransmission to the pig bladder neck: role of KATP channels, sensory nerves and calcium signaling. J Urol. 2013;190(2):746-56.
Fernandes, V. S., Ribeiro, A. S., Barahona, M. V., Orensanz, L. M., Martínez-Sáenz, A., Recio, P., Martínez, A. C., Bustamante, S., Carballido, J., García-Sacristán, A., Prieto, D., & Hernández, M. (2013). Hydrogen sulfide mediated inhibitory neurotransmission to the pig bladder neck: role of KATP channels, sensory nerves and calcium signaling. The Journal of Urology, 190(2), 746-56. https://doi.org/10.1016/j.juro.2013.02.103
Fernandes VS, et al. Hydrogen Sulfide Mediated Inhibitory Neurotransmission to the Pig Bladder Neck: Role of KATP Channels, Sensory Nerves and Calcium Signaling. J Urol. 2013;190(2):746-56. PubMed PMID: 23454157.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen sulfide mediated inhibitory neurotransmission to the pig bladder neck: role of KATP channels, sensory nerves and calcium signaling. AU - Fernandes,Vítor S, AU - Ribeiro,Ana S F, AU - Barahona,María Victoria, AU - Orensanz,Luis M, AU - Martínez-Sáenz,Ana, AU - Recio,Paz, AU - Martínez,Ana Cristina, AU - Bustamante,Salvador, AU - Carballido,Joaquín, AU - García-Sacristán,Albino, AU - Prieto,Dolores, AU - Hernández,Medardo, Y1 - 2013/02/28/ PY - 2013/02/21/received PY - 2013/02/21/accepted PY - 2013/3/5/entrez PY - 2013/3/5/pubmed PY - 2013/11/14/medline KW - 4-AP KW - 4-aminopyridine KW - AM KW - ATP KW - ATP dependent K(+) KW - CGRP KW - COX KW - CSE KW - CSPA KW - Ca(2+) activated K(+) KW - Emax KW - K(ATP) KW - K(Ca) KW - K(V) KW - KPSS KW - L-NOARG KW - MLCP KW - N(G)-nitro-L-arginine KW - NO KW - PACAP KW - PKA KW - PSS KW - TRPA(1) KW - TRPV(1) KW - VOC KW - VPAC KW - [Ca(2+)](i) KW - acetoxymethyl ester KW - adenosine 5′-triphosphate KW - calcitonin gene-related peptide KW - capsaicin sensitive primary afferent KW - cyclooxygenase KW - cystathionine γ-lyase KW - hydrogen sulfide KW - intracellular Ca(2+) KW - maximum response KW - muscle, smooth KW - myosin light chain phosphatase KW - nitric oxide KW - physiological saline solution KW - pituitary adenylyl cyclase activating polypeptide KW - potassium channels KW - potassium rich PSS KW - protein kinase A KW - synaptic transmission KW - transient receptor potential A1 KW - transient receptor potential vanilloid 1 KW - urinary bladder KW - vasoactive intestinal peptide receptor KW - voltage gated Ca(2+) KW - voltage gated K(+) SP - 746 EP - 56 JF - The Journal of urology JO - J Urol VL - 190 IS - 2 N2 - PURPOSE: Because neuronal released endogenous H2S has a key role in relaxation of the bladder outflow region, we investigated the mechanisms involved in H2S dependent inhibitory neurotransmission to the pig bladder neck. MATERIALS AND METHODS: Bladder neck strips were mounted in myographs for isometric force recording and simultaneous measurement of intracellular Ca(2+) and tension. RESULTS: On phenylephrine contracted preparations electrical field stimulation and the H2S donor GYY4137 evoked frequency and concentration dependent relaxation, which was reduced by desensitizing capsaicin sensitive primary afferents with capsaicin, and the blockade of adenosine 5'-triphosphate dependent K(+) channels, cyclooxygenase and cyclooxygenase-1 with glibenclamide, indomethacin and SC560, respectively. Inhibition of vanilloid, transient receptor potential A1, transient receptor potential vanilloid 1, vasoactive intestinal peptide/pituitary adenylyl cyclase-activating polypeptide and calcitonin gene-related peptide receptors with capsazepine, HC030031, AMG9810, PACAP6-38 and CGRP8-37, respectively, also decreased electrical field stimulation and GYY4137 responses. H2S relaxation was not changed by guanylyl cyclase, protein kinase A, or Ca(2+) activated or voltage gated K(+) channel inhibitors. GYY4137 inhibited the contractions induced by phenylephrine and by K(+) enriched (80 mM) physiological saline solution. To a lesser extent it decreased the phenylephrine and K(+) induced increases in intracellular Ca(2+). CONCLUSIONS: H2S produces pig bladder neck relaxation via activation of adenosine 5'-triphosphate dependent K(+) channel and by smooth muscle intracellular Ca(2+) desensitization dependent mechanisms. H2S also promotes the release of sensory neuropeptides and cyclooxygenase-1 pathway derived prostanoids from capsaicin sensitive primary afferents via transient receptor potential A1, transient receptor potential vanilloid 1 and/or related ion channel activation. SN - 1527-3792 UR - https://www.unboundmedicine.com/medline/citation/23454157/Hydrogen_sulfide_mediated_inhibitory_neurotransmission_to_the_pig_bladder_neck:_role_of_KATP_channels_sensory_nerves_and_calcium_signaling_ L2 - https://www.jurology.com/doi/10.1016/j.juro.2013.02.103?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -