Conflicts of interest: none.
Original Basic Science Article
Article first published online: 23 JUL 2010
Copyright © 2010 Wiley-Liss, Inc.
Neurourology and Urodynamics
Volume 30, Issue 1, pages 151–157, January 2011
How to Cite
Martínez-Saénz, A., Barahona, M. V., Orensanz, L. M., Recio, P., Bustamante, S., Benedito, S., Carballido, J., García-Sacristán, A., Prieto, D. and Hernández, M. (2011), Mechanisms involved in the nitric oxide independent inhibitory neurotransmission to the pig urinary bladder neck. Neurourol. Urodyn., 30: 151–157. doi: 10.1002/nau.20960
Karl-Erik Andersson led the review process.
- Issue published online: 22 DEC 2010
- Article first published online: 23 JUL 2010
- Manuscript Accepted: 19 MAY 2010
- Manuscript Received: 16 MAR 2010
- Ministerio de Ciencia e Innovación, Spain. Grant Number: PS09/00044
- adenylyl cyclase;
- guanylyl cyclase;
- K+ channels;
- Na+–K+ ATPase;
- non-nitrergic inhibitory transmission;
- pig bladder neck
The current study investigates the mechanisms involved in nitric oxide (NO)-independent, nonadrenergic, noncholinergic (NANC) inhibitory neurotransmission to the pig urinary bladder neck.
Urothelium-denuded strips were mounted in organ baths containing physiological saline solution (PSS) at 37°C for isometric force recordings. The relaxations to electrical field stimulation (EFS) were carried out on strips treated with guanethidine, atropine and NG-nitro-L-arginine, to block noradrenergic neurotransmission, muscarinic receptors and NO synthase, respectively, and precontracted with phenylephrine.
EFS (1–16 Hz) produced frequency-dependent relaxations which were abolished by the blockade of neuronal voltage-activated Na+ channels. Nonselective and selective inhibition of COX and COX-1, respectively, and blockade of Na+–K+ ATPase reduced the EFS-induced relaxations. However, blockade of COX-2, soluble guanylyl cyclase, large-, intermediate- and small-conductance Ca2+-activated K+ channels, ATP-dependent K+ channels, voltage-gated K+ channels, cAMPc-dependent protein kinase (PKA) and cGMP-dependent protein kinase (PKG) failed to modify the nerve-mediated relaxations.
The NO-independent inhibitory neurotransmission to the pig urinary bladder neck is mediated, in part, through prostanoids release from a COX-1 pathway, and through activation of the Na+–K+ ATPase. PKA and PKG pathways and postjunctional K+ channels do not appear to be involved in the NO-independent nerve-mediated relaxations. Neurourol. Urodyn. 30:151–157, 2011. © 2010 Wiley-Liss, Inc.