Person: Recio Visedo, María Paz
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First Name
María Paz
Last Name
Recio Visedo
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Farmacia
Department
Fisiología
Area
Fisiología
Identifiers
5 results
Search Results
Now showing 1 - 5 of 5
Item Role of neuronal voltage‐gated K+ channels in the modulation of the nitrergic neurotransmission of the pig urinary bladder neck(British Journal of Pharmacology, 2008) Hernández Martín, Marina; Barahona Gomáriz, María Victoria; Recio Visedo, María Paz; Navarro Dorado, Jorge; Bustamante Alarma, Salvador; Benedito Castellote, Sara; García Sacristán, Albino; Prieto Ocejo, Dolores; Orensanz Muñoz, Luis MiguelBackground 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.Item Noradrenergic vasoconstriction of pig prostatic small arteries(Naunyn-Schmiedeberg’s Arch Pharmacol, 2008) Recio Visedo, María Paz; Orensanz Muñoz, Luis Miguel; Martínez Sainz, María Del Pilar; Navarro Dorado, Jorge; Bustamante Alarma, Salvador; García Sacristán, Albino; Prieto Ocejo, Dolores; Hernández Rodríguez, Medardo VicenteThe current study investigated the distribution of adrenergic nerves and the action induced by noradrenaline (NA) in pig prostatic small arteries. Noradrenergic innervation was visualized using an antibody against dopamine-beta-hydroxylase (DBH), and the NA effect was studied in small arterial rings mounted in microvascular myographs for isometric force recordings. DBH-immunoreactive nerve fibers were located at the adventitia and the adventitia-media border of the vascular wall. Electrical field stimulation (EFS, 1-32 Hz) evoked frequency-dependent contractions that were reduced by guanethidine and prazosin (adrenergic neurotransmission and α1-adrenoceptors blockers, respectively) and by the α2-adrenoceptor agonist UK 14,304. The α2-adrenoceptor antagonist rauwolscine reversed the UK 14,304-produced inhibition. NA produced endothelium-independent contractions that were antagonized with low estimated affinities and Schild slopes different from unity by prazosin and the α1A-adrenoceptor antagonist N-[2-(2-cyclopropylmethoxyphenoxy) ethyl]-5-chloro-α-α-dimethyl-1H-indole-3-ethanamine (RS 17053). The α1A-adrenoceptor antagonist 5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl]propyl]-2,4-(1H)-pyrimidinedione (RS 100329), which also displays high affinity for α1L-adrenoceptors, and the α1L-adrenoceptor antagonist tamsulosin, which also has high affinity for α1A- and α1D-adrenoceptors, induced rightward shifts with high affinity of the contraction-response curve to NA. The α1D-adrenoceptor antagonist 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]-ethyl]8-azaspiro[4,5]decane-7,9-dione dihydrochloride (BMY 7378) failed to modify the NA contractions that were inhibited by extracellular Ca2+ removal and by voltage-activated (L-type) Ca2+ channel blockade. These data suggest that pig prostatic resistance arteries have a rich noradrenergic innervation; and NA, whose release is modulated by prejunctional α2-adrenoceptors, evokes contraction mainly through activation of muscle α1L-adrenoceptors coupled to extracellular Ca2+ entry via voltage (L-type)- and non-voltage-activated Ca2+ channels.Item Neuronal and non-neuronal bradykinin receptors are involved in the contraction and/or relaxation to the pig bladder neck smooth muscle(Neurourology and urodynamics, 2013) Ribeiro, Ana Sofía Fernandes; Leite Fernandes, Vitor Samuel; Martínez Sainz, María Del Pilar; Martínez-Sáenz, Ana; Pazos Rodríguez, María Ruth; Orensanz Muñoz, Luis Miguel; Recio Visedo, María Paz; Bustamante Alarma, Salvador; Carballido Rodríguez, Joaquín; García Sacristán, Albino; Prieto Ocejo, Dolores; Hernández Rodríguez, Medardo VicenteAims: The current study investigates the role played by bradykinin (BK) receptors in the contractility to the pig bladder neck smooth muscle. Methods: Bladder neck strips were mounted in myographs for isometric force recordings and BK receptors expression was also determined by immunohistochemistry. Results: B2 receptor expression was observed in the muscular layer and urothelium whereas B1 expression was consistent detected in urothelium. A strong B2 immunoreactivity was also observed within nerve fibers among smooth muscle bundles. On urothelium-denuded preparations basal tone, BK induced concentration-dependent contractions which were reduced in urothelium-intact samples, by extracellular Ca(2+) removal and by blockade of B2 receptors and voltage-gated Ca(2+) (VOC) and non-VOC channels, and increased by cyclooxygenase (COX) inhibition. On phenylephrine-precontracted denuded strips, under non-adrenergic non-cholinergic (NANC) conditions, electrical field stimulation-elicited frequency-dependent relaxations which were reduced by B2 receptor blockade. In urothelium-intact samples, the B1 receptor agonist kallidin promoted concentration-dependent relaxations which were reduced by blockade of B1 receptors, COX, COX-1 and large-conductance Ca(2+) -activated K(+) (BKCa ) channels and abolished in urothelium-denuded samples and in K(+) -enriched physiological saline solution-precontracted strips. Conclusions: These results suggest that BK produces contraction of pig bladder neck via smooth muscle B2 receptors coupled to extracellular Ca(2+) entry via VOC and non-VOC channels with a minor role for intracellular Ca(2+) mobilization. Facilitatory neuronal B2 receptors modulating NANC inhibitory neurotransmission and urothelial B1 receptors producing relaxation via the COX-1 pathway and BKCa channel opening are also demonstrated.Item Mechanisms involved in testosterone-induced vasodilatation in pig prostatic small arteries(Life Sciences, 2008) Navarro Dorado, Jorge; Orensanz Muñoz, Luis Miguel; Recio Visedo, María Paz; Bustamante Alarma, Salvador; Benedito Castellote, Sara; Martínez Gómez, Ana Cristina; García Sacristán, Albino; Prieto Ocejo, Dolores; Hernández Rodríguez, Medardo VicenteAims: Testosterone is beneficial to the cardiovascular system due to its direct coronary vasodilatory action and its circulatory deficiency is associated with coronary artery disease (CAD), which has been proposed as an extrinsic risk factor for benign prostatic hyperplasia (BPH). Therefore, the current study investigated the mechanisms involved in the testosterone-induced vasodilatation in pig prostatic small arteries. Main methods: The testosterone vasoactive effects were assessed in small arterial rings mounted in micro- vascular myographs for isometric force recordings. Key findings: Testosterone and the non-aromatizable metabolite 4, 5α-dihydrotestosterone (DHT) evoked a similar concentration-dependent relaxation on noradrenaline (NA)-precontracted rings. Similar responses were obtained in preparations contracted with 60 mM K+-enriched physiological saline solution. Endothelium mechanical removal or pre-treatment with blockers of nitric oxide (NO) synthase, guanylate cyclase, aromatase activity, intracellular androgenic receptor (AR), 5α-reductase, prostanoid synthesis and K+ channels, failed to modify the responses to testosterone. In Ca2+-free 124 mM KPSS, testosterone markedly inhibited in a concentration-dependent manner the contraction curve t °CaCl2. In arteries pretreated with an L-type voltage-activated Ca2+ channels (VOCCs) inhibitor, nifedipine, testosterone still relaxed noradrenaline- precontracted arteries. Significance: These data suggest that testosterone induces a direct vasodilatory action in pig prostatic small arteries independent of either endothelium, NO, prostanoids, aromatase or 5α-reductase activities, AR or K+ channels. Such an effect is suggested to be produced via blockade of extracellular Ca2+ entry through L-type VOCCs and non-L-type Ca2+ channels. Testosterone-induced vasodilatation could be useful to prevent prostatic ischemia.Item Endogenous Hydrogen Sulfide has a Powerful Role in Inhibitory Neurotransmission to the Pig Bladder Neck(Journal of Urology, 2013) Leite Fernandes, Vitor Samuel; Ribeiro, Ana S.F.; Martínez, María Pilar; Orensanz, Luis M.; Barahona Gomáriz, María Victoria; Martínez-Sáenz, Ana; Recio Visedo, María Paz; Benedito Castellote, Sara; Bustamante, Salvador; Carballido, Joaquín; García Sacristán, Albino; Prieto Ocejo, Dolores; Hernández Rodríguez, Medardo VicentePurpose: We investigated the possible involvement of H2S in nitric oxide independent inhibitory neurotransmission to the pig bladder neck. Materials and methods: We used immunohistochemistry to determine the expression of the H2S synthesis enzymes cystathionine γ-lyase and cystathionine β-synthase. We also used electrical field stimulation and myographs for isometric force recordings to study relaxation in response to endogenously released or exogenously applied H2S in urothelium denuded, phenylephrine precontracted bladder neck strips under noradrenergic, noncholinergic, nonnitrergic conditions. Results: Cystathionine γ-lyase and cystathionine β-synthase expression was observed in nerve fibers in the smooth muscle layer. Cystathionine γ-lyase and cystathionine β-synthase immunoreactive fibers were also identified around the small arteries supplying the bladder neck. Electrical field stimulation (2 to 16 Hz) evoked frequency dependent relaxation, which was decreased by DL-propargylglycine and abolished by tetrodotoxin (blockers of cystathionine γ-lyase and neuronal voltage gated Na(+) channels, respectively). The cystathionine β-synthase inhibitor O-(carboxymethyl)hydroxylamine did not change nerve mediated responses. The H2S donor GYY4137 (0.1 nM to 10 μM) induced potent, concentration dependent relaxation, which was not modified by neuronal voltage gated Na(+) channels, or cystathionine γ-lyase or cystathionine β-synthase blockade. Conclusions: Results suggest that endogenous H2S synthesized by cystathionine γ-lyase and released from intramural nerves acts as a powerful signaling molecule in nitric oxide independent inhibitory transmission to the pig bladder neck.