H2S与膀胱颈功能：猪模型
作者：Vítor S. Fernandes, Ana S.F. Ribeiro, María Victoria Barahona, Luis M. Orensanz, et al. 来源：Journal of Urology 日期：2013-03-12
导读
Hydrogen sulfide-mediated inhibitory neurotransmission to the pig bladder neck: Role of K ATP channels, sensory nerves and calcium signaling
Abstract
Purpose
As neuronal-released endogenous hydrogen sulfide (H2S) plays a key role in the relaxation of the bladder outflow region, this study investigates 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 recordings and simultaneous measurements of intracellular Ca2+ concentration ([Ca2+]i) and tension.
Results
On phenylephrine-contracted preparations, electrical field stimulation (EFS) and the H2S donor GYY4137 evoked frequency- and concentration-dependent relaxations which were reduced by desensitization of capsaicin-sensitive primary afferents (CSPA) with capsaicin and blockade of ATP-dependent K+ (KATP) channels, cyclooxygenase (COX) and cyclooxygenase-1 (COX-1) with glibenclamide, indomethacin and SC560, respectively. Inhibition of vanilloid, transient receptor potential A1 (TRPA1), transient receptor potential vanilloid 1 (TRPV1), vasoactive intestinal peptide/pituitary adenylyl cyclase-activating polypeptide (VIP/PACAP) and calcitonin gene-related peptide (CGRP) receptors with capsazepine, HC030031, AMG9810, PACAP6-38 and CGRP8-37, respectively, also reduced EFS and GYY4137 responses. H2S relaxations were not changed by guanylyl cyclase, protein kinase A (PKA), Ca2+-activated K+ (KCa) channel or voltage-gated K+ (Kv) channel inhibitors. GYY4137 inhibited the contractions induced by PhE and by K+-enriched (80 mM) physiological saline solution and reduced to a lesser extent the PhE- and K+-induced increases in [Ca2+] i.
Conclusions
H2S produces relaxation of pig bladder neck via activation of KATP channel and also by smooth muscle [Ca2+] i desensitization-dependent mechanisms. H2S also promotes the release of sensory neuropeptides and of COX-1 pathway-derived prostanoids from CSPA, through TRPA1, TRPV1 and/or related ion channel activation.
http://www.jurology.com/article/S0022-5347(13)00379-0/abstract
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