Navegando por Palavras-chave "vas deferens"

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    Decreased noradrenergic and serotonergic reactivity of vas deferens of newborn rats from mothers treated with the serotonin reuptake inhibitor fluoxetine during pregnancy and breast-feeding
    (Elsevier B.V., 2007-11-10) Pereira, Janaina D.; Caricati-Neto, Afonso [UNIFESP]; Jurkiewicz, Aron; Jurkiewicz, Neide H.; Universidade Federal de São Paulo (UNIFESP)
    Female Wistar rats were treated with the serotonin reuptake inhibitor fluoxetine (10 mg/kg/i.p/day), during pregnancy and breast-feeding, for the study of the corresponding newborn rats. At the end of the prewcaning period, the 30-day old litters had their vas deferens removed for testing peripheral sympathetic reactivity, through the following experiments in vitro: (a) concentration-contraction curves for serotonin and for the adrenergic agonists noradrenaline, phenylephrine, clonidine and dopamine or for the indirect agonist tyramine (b) contractions induced by electric field stimulation, as an indicator of sympathetic neurotransmission (c) release of endogenous noradrenaline, measured by real-time determinations on HPLC (d) Ca+2 time-contraction curves, to check for changes on Ca+2 translocation. Our results showed that the affinity (pD(2)) for serotonin was strikingly decreased by about 1.5 log units. the pD2 for adrenergic agonists was decreased by about 0.5 log units, except for dopamine and clonidine. the maximum effects and intrinsic activity were decreased only for dopamine. On the other hand, the response to Ca+2 and the release of noradrenaline from nerve terminals were not modified. in additional experiments, the mother's body weights were measured, showing a decrease during gestation and a recovery during lactation while the offspring's weights were lower than controls. It is concluded that, besides the alterations on body weights, changes on noradrenergic and serotonergic mechanisms were observed and persisted in the newborn, at least one month after parturition. (c) 2007 Elsevier Inc. All rights reserved.
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    Effects of indoramin in rat vas deferens and aorta: concomitant alpha(1)-adrenoceptor and neuronal uptake blockade
    (Stockton Press, 1999-08-01) Pupo, André S.; Cavenaghi, Daniela LC; Campos, Marcelo; Morais, Paola D.; Jurkiewicz, Neide Hyppolito [UNIFESP]; Jurkiewicz, Aron [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    1 the actions of the alpha(1)-adrenoceptor antagonist indoramin have been examined against the contractions induced by noradrenaline in the rat vas deferens and aorta taking into account a putative neuronal uptake blocking activity of this antagonist which could. result in self-cancelling actions.2 Indoramin behaved as a simple competitive antagonist of the contractions induced by noradrenaline in the vas deferens and aorta yielding pA(2) values of 7.38 +/- 0.05 (slope = 0.98 +/- 0.03) and 6.78 +/- 0.14 (slope = 1.08 +/- 0.06), respectively.3 When the experiments were repeated in the presence of cocaine (6 mu M) the potency (pA(2)) of indoramin in antagonizing the contractions of the vas deferens to noradrenaline was increased to 8.72 +/- 0.07 (slope = 1.10 +/- 0.05) while its potency remained unchanged in the aorta (pA(2) = 6.69 +/- 0.12; slope = 1.04 +/- 0.05).4 in denervated vas deferens, indoramin antagonized the contractions to noradrenaline with a potency similar to that found in the presence of cocaine (8.79 +/- 0.07; slope = 1.09 +/- 0.06).5 It is suggested that indoramin blocks alpha(1)-adrenoceptors and neuronal uptake in rat vas deferens resulting in Schild plots with slopes not different from unity even in the absence of selective inhibition of neuronal uptake. As a major consequence of this double mechanism of action, the pA(2) values for this antagonist are underestimated when calculated in situations where the neuronal uptake is active, yielding spurious pK(B) values.
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    Enhancement of purinergic neurotransmission by galantamine and other acetylcholinesterase inhibitors in the rat vas deferens
    (Elsevier B.V., 2004-10-25) Caricati-Neto, A.; D'angelo, LCA; Reuter, H.; Jurkiewicz, N. H.; Garcia, A. G.; Jurkiewicz, A.; Universidade Federal de São Paulo (UNIFESP); Univ Autonoma Madrid; Hosp Princesa
    Galantamine, a mild acetylcholinesterase inhibitor and an allosteric ligand of nicotinic receptors, enhanced in a concentration-dependent manner the amplitude of purinergic twitch contractions of the electrically stimulated rat vas deferens (0.2 Hz, 1 ms, 60 V). Other acetylcholinesterase inhibitors also increased the twitches, showing a hierarchy of potencies of galantamine>physostigmine >tacrine>rivastigmine=donepezil. the potentiations seem to be unrelated to the ability to inhibit acetylcholinesterase, since the hierarchy of potencies to block the enzyme in vas deferens was tacrine>physostigmine>rivastigmine>donepezil>galantamine. Acetylcholine also increased the twitches; such effect was produced by a low range of concentrations of acetylcholine (10(-10)-10(-7) M). This facilitatory effect of acetylcholine on twitches was significantly potentiated by galantamine (10(-7)-10(-6) M), but not by rivastigmine or donepezil. A striking enhancement of twitches was also caused by charybdotoxin, a blocker of high-conductance Ca2+-activated K+ channels, and by 4-aminopyridine, a non-specific blocker of K+ channels; in addition, apamin, a blocker of small-conductance Ca2+-activated K+ channels, induced a lower potentiation. the antagonist mecamylamine (10(-7)-10(-6) M) reduced by 80% the potentiation by galantamine, indicating the involvement of nicotinic receptors. Therefore, it is suggested that, besides an inhibition of acetylcholinesterase, some additional mechanisms, such as blockade of Ca2+-dependent K+ channels, or activation of nicotinic receptors of nerve terminals, might be involved in twitch potentiation. These results are relevant in the context of the clinical use of galantamine to improve cognition and behaviour in patients with Alzheimer's disease. (C) 2004 Elsevier B.V. All rights reserved.
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    Functional properties of agmatine in rat vas deferens
    (Elsevier B.V., 1996-07-04) Jurkiewicz, N. H.; doCarmo, L. G.; Hirata, H.; Santos, W. D.; Jurkiewicz, A.; Universidade Federal de São Paulo (UNIFESP)
    Experiments were performed with rat vas deferens to verify whether agmatine, an endogenous ligand for adrenoceptors and imidazoline receptors, can influence sympathetic neurotransmission, with respect to contractions induced by transmural nerve stimulation, contractions induced by exogenous noradrenaline, and overflow of endogenous noradrenaline. It was shown that agmatine (a) caused a dose-dependent potentiation of electrically induced twitches, up to about 70% in relation to controls, (b) shifted to the right the inhibitory concentration-response curves for clonidine on electrically induced twitches, indicating competitive antagonism at presynaptic ol-adrenoceptors, with a pA(2) value of 4.12 +/- 0.10, (c) shifted to the right the concentration-response curves for noradrenaline-induced contractions, indicating competitive antagonism at postsynaptic alpha-adrenoceptors as well, with a pA(2) value of 4.03 +/- 0.10, and (d) caused a dose-dependent increase of KCl-induced overflow of noradrenaline, up to about 90% in relation to controls. It is concluded that agmatine has multiple effects on sympathetic neurotransmission in rat vas deferens.
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    omega-Conotoxins block neurotransmission in the rat vas deferens by binding to different presynaptic sites on the N-type Ca2+ channel
    (Elsevier B.V., 1997-02-26) Hirata, H.; Albillos, A.; Fernandez, F.; Medrano, J.; Jurkiewicz, A.; Garcia, A. G.; UNIV AUTONOMA MADRID; Universidade Federal de São Paulo (UNIFESP)
    Electrically-induced twitch responses of the prostatic segment of vas deferens (0.1 Hz, 65 V, 1 ms) are mainly due to the transient presynaptic release of ATP, which acts postsynaptically on non-adrenergic receptors to contract smooth muscle cells. These responses were fully blocked by nanomolar concentrations of the omega-conotoxins GVIA, MVIIA, and MVIIC, most likely by inhibiting Ca2+ entry through presynaptic N-type Ca2+ channels controlling the release of ATP. Repeated washout of the toxins allowed the recovery of contractions, except for omega-conotoxin GVIA, whose inhibitory effects remained unchanged for at least 60 min. in addition, micromolar concentrations of omega-conotoxin MVIIC were unable to protect against the irreversible inhibition of twitch contractions induced by nanomolar concentrations of omega-conotoxin GVIA, At low extracellular Ca2+ concentrations (1.5 mM), 20 nM of omega-conotoxin GVIA or MVIIA inhibited completely the twitch contractions in about 10 min. in 5 mM Ca2+ the blockade of twitch contractions after 10 min was 70% for both toxins. in 1.5 mM Ca2+ omega-conotoxin MVIIC (1 mu M) inhibited completely the twitch contraction after 10 min. in 5 mM Ca2+ blockade developed very slowly and was very poor after 30 min, omega-conotoxin MVIIC depressed the response by only 20%. These results are compatible with the idea that the three omega-conotoxins block the purinergic neurotransmission of the vas deferens by acting on presynaptic N-type voltage-dependent Ca2+ channels. However, omega-conotoxin MVIIC seems to bind to sites different from those recognised by omega-conotoxin GVIA and MVIIA, which are markedly differentiated by their Ca2+ requirements for binding to their receptors.
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    Scanning electron microscopy of vas deferens epithelium after temporary alteration caused by radiopaque medium
    (Hemisphere Publ Corp, 1998-03-01) Hayashi, Hisakazu [UNIFESP]; Giovanoni, Marisa [UNIFESP]; Giusti, Guilherme [UNIFESP]; Molina, W. R.; Universidade Federal de São Paulo (UNIFESP)
    Nine male rats (Rattus norvegicus albinus) weighing approximately 300 g were divided into 3 groups: a control group (CG), an experimental group of 7 days (EG-7), and an experimental group of 35 days (EG-35). All rats except those in the control group underwent a left vasography. The EG-7 and EG-35 rats were killed on the 7th and 35th days, respectively, after vasography; CG rats were killed on a randomly chosen day. The histological sections and scanning electromicrographs showed that the temporary alterations caused by radiopaque medium on vas deferens mucosa seen on the 7th day after vasography were completely repaired on the 35th day of recovery and either apical secretion or stereocilia of principal cells were reestablished.
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    TTX-sensitive Na+ and nifedipine-sensitive Ca2+ channels in rat vas deferens smooth muscle cells
    (Elsevier B.V., 1999-07-15) Belevych, A. E.; Zima, A. V.; Vladimirova, I. A.; Hirata, Hanako [UNIFESP]; Jurkiewicz, Aron [UNIFESP]; Jurkiewicz, Neide Hyppolito [UNIFESP]; Shuba, M. F.; Natl Acad Sci Ukraine; Universidade Federal de São Paulo (UNIFESP)
    The inward currents in single smooth muscle cells (SMC) isolated from epididymal part of rat vas deferens have been studied using whole-cell patch-clamp method. Depolarising steps from holding potential -90 mV evoked inward current with fast and slow components. the component with slow activation possessed voltage-dependent and pharmacological properties characteristic for Ca2+ current carried through L-type calcium channels (I-Ca). the fast component of inward current was activated at around -40 mV, reached its peak at 0 mV, and disappeared upon removal of Na ions from bath solution. This current was blocked in dose-dependent manner by tetrodotoxin (TTX) with an apparent dissociation constant of 6.7 nM. On the basis of voltage-dependent characteristics, TTX sensitivity of fast component of inward current and its disappearance in Na-free solution it is suggested that this current is TTX-sensitive depolarisation activated sodium current (I-Na) Cell dialysis with a pipette solution containing no macroergic compounds resulted in significant inhibition of I-Ca (depression of peak I-Ca by about 81% was observed by 13 min of dialysis), while I-Na remained unaffected during 50 min of dialysis. These data draw first evidence for the existence of TTX-sensitive Na+ current in single SMC isolated from rat vas deferens. These Na+ channels do not appear to be regulated by a phosphorylation process under resting conditions. (C) 1999 Elsevier Science B.V. All rights reserved.
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    Up-regulation of Ca2+ channels in vas deferens after chronic treatment of newborn rats with nifedipine
    (Elsevier B.V., 2002-05-17) Verde, L. F.; Lafayette, SSL; Caricati-Neto, A.; Jurkiewicz, N. H.; Jurkiewicz, A.; Universidade Federal de São Paulo (UNIFESP)
    Radioligand binding and contraction techniques were used to verify if L-type Ca2+ charnels are modified in rat vas deferens after treatment with the blocker nifedipine (15 mug), injected at 7, 14, 21 and 28 days after birth. Vas deferens tissue was used 10, 30 and 90 days after the last injection, to verify if modifications are persistent. Binding studies with cell membranes, using [H-3]isradipine, showed an increase of the density (B-max) of Ca2+ channels by more than 60%, after 10 and 30 days, without changes of affinity (K-d). Maximal contractions (E-max) of KCl, were increased by 106% and 37%, respectively, after 10 and 30 days, without changes of apparent affinity (pD(2)). After 90 days, the values of B-max, K-d, E-max and pD(2) were not different from the controls. Differences were also not found for rats injected when adult. It is concluded that treatment of newborn, but not of adult, rats with nifedipine produced a long-lasting, though reversible, upregulation of L-type Ca2+ channels. (C) 2002 Elsevier Science B.V. All rights reserved.
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    Use of transgenic (knockout) mice reveals a site distinct from the alpha(2A)-adrenoceptors for agmatine in the vas deferens
    (Polish Acad Sciences Inst Pharmacology, 2009-03-01) Santos, Wilson da Costa; Garcez-do-Carmo, Lucia [UNIFESP]; Silva, Eliane Cristina da [UNIFESP]; Pascual, Ricardo de; Jurkiewicz, Neide Hyppolito [UNIFESP]; Jurkiewicz, Aron [UNIFESP]; Gandia, Luis; Universidade Federal Fluminense (UFF); Universidade Federal de São Paulo (UNIFESP); Fac Med
    The inhibitory effect of agmatine on electrically induced contractions was studied in vas deferens of Adra 2a transgenic mice lacking alpha(2A)-adrenoceptors. Agmatine and clonidine caused a concentration-dependent inhibition of twitches. However, while agmatine showed a similar pIC(50) value in control and transgenic mice, the pIC(50) value for clonidine was about 30-fold lower in knockout mice. In both strains, yohimbine shifted the curve for clonidine, but not for agmatine, even when a 100-fold higher concentration of yohimbine was employed. Our results indicate that inhibition by agmatine in mouse vas deferens is not simply due to interactions with alpha(2)-adrenoceptors in our experimental conditions.
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    Voltage-gated potassium currents in rat vas deferens smooth muscle cells
    (Springer, 2003-06-01) Harhun, M. I.; Jurkiewicz, A.; Jurkiewicz, N. H.; Kryshtal, D. O.; Shuba, M. F.; Vladimirova, I. A.; Bogomoletz Inst Physiol; Universidade Federal de São Paulo (UNIFESP)
    Voltage-gated components of the outward current in single smooth muscle cells isolated from the epididymal part of the rat vas deferens were studied using amphotericin B perforated patch-clamp techniques. the complex kinetics of the net outward current elicited by positive voltage steps from -80 mV to +40 mV suggested the presence of several components. Bath application of 200 nM charybdotoxin, a potent blocker of large-conductance, Ca2+-dependent K+ channels (BKCa), reduced the current amplitude significantly. When BKCa channels were suppressed, fast-inactivating (I-K,I-f) and delayed rectifying (I-K,I-dr) components of the outward current were identified. I-K,I-f was characterized by fast kinetics of current decay, negative steady-state activation and inactivation dependencies and sensitivity to 4-aminopyridine with an apparent K-d of 0.32 mM, properties similar to those of the A-type K+ current. in contrast, I-K,I-dr activated and inactivated at more positive potentials. the time constant of activation of I-K,I-dr was voltage dependent with an e-fold decrease per 21 mV depolarization. I-K,I-dr was inhibited by clofilium, a blocker of voltage-gated K+ channels, with an IC50 of 12 muM and was not blocked by 5 mM 4-aminopyridine. the possible significance of the voltage-gated currents is discussed.