Person:
Hernández Martín, Marina

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First Name
Marina
Last Name
Hernández Martín
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Farmacia
Department
Fisiología
Area
Fisiología
Identifiers
UCM identifier

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  • Publication
    Role of neuronal voltage‐gated K+ channels in the modulation of the nitrergic neurotransmission of the pig urinary bladder neck
    (2008-03) Hernández Martín, Marina; Barahona Gomáriz, María Victoria; Recio Visedo, María Paz; Navarro Dorado, Jorge; Bustamante, S.; Benedito Castellote, Sara; García Sacristán, Albino; Prieto Ocejo, Dolores; Orensanz Muñoz, Luis Miguel
    Background and purpose: As nitric oxide (NO) plays an essential role in the inhibitory neurotransmission of the bladder neck of several species, the current study investigates the mechanisms underlying the NO‐induced relaxations in the pig urinary bladder neck.Experimental approach:Urothelium‐denuded bladder neck strips were dissected and mounted in isolated organ baths containing a physiological saline solution at 37 °C and continuously gassed with 5% CO2and 95% O2, for isometric force recording. The relaxations to transmural nerve stimulation (EFS), or to exogenously applied acidified NaNO solution were carried out on strips pre‐contracted with phenylephrine, and treated with guanethidine and atropine, to block noradrenergic neurotransmission and muscarinic receptors, respectively.Key results:EFS (0.2–1 Hz) and addition of acidified NaNO solution (1 μM–1 mM) evoked frequency‐ and concentration‐dependent relaxations, respectively. These responses were potently reduced by the blockade of guanylate cyclase and were not modified by the K+ channel blockers iberiotoxin, charybdotoxin, apamin or glibenclamide. The voltage‐gated K+ (Kv) channels inhibitor 4‐aminopyridine, greatly enhanced the nitrergic relaxations evoked by EFS, but did not affect the NaNO2 solution‐induced relaxations.Conclusions and implications:NO, whose release is modulated by pre‐junctional Kv channels, relaxes the pig urinary bladder neck through a mechanism dependent on the activation of guanylate cyclase, in which post‐junctional K+ channels do not seem to be involved. Modulation of Kv channels could be useful in the therapy of the urinary incontinence produced by intrinsic sphincteric deficiency.