• adenylyl cyclase;
  • cyclooxygenase;
  • EFS;
  • 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.