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Demoraes S - One of the best experts on this subject based on the ideXlab platform.

  • SUBSENSITIVITY TO BETA-ADRENOCEPTOR AGONISTS IN PACEMAKERS ISOLATED FROM SENESCENT RATS
    'Elsevier BV', 2015
    Co-Authors: Rc Spadari, Demoraes S
    Abstract:

    1. The effects of aging on the responsiveness of the isolated pacemaker of the rat to the chronotropic effect of norepinephrine, isoproterenol and Soterenol were studied. 2. Pacemakers isolated from senescent rats (22-24 months old) showed subsensitivity to norepinephrine, isoproterenol and Soterenol, when compared with pacemakers isolated from young rats (3-4 months old). The maximum response to the partial agonist Soterenol was reduced. 3. Determination of the pA2 value of metoprolol in pacemakers isolated from senescent and young rats showed that the chronotropic response is mediated by a homogeneous beta-1-adrenoceptor population. 4. Inhibition of extraneuronal uptake did not potentiate the chronotropic effect of isoproterenol in pacemakers isolated from senescent rats. Addition of cocaine shifted the concentration-effect curve for norepinephrine only 2.2-fold to the left in senescent rats. 5. It is concluded that, during aging, impairment of the extraneuronal and neuronal uptake mechanisms has an important role in the control of chronotropic responsiveness to catecholamines.22591792

  • Subsensitivity To Beta-adrenoceptor Agonists In Right Atria Isolated From Footshock-stressed Rats.
    2015
    Co-Authors: Bassani R A, Demoraes S
    Abstract:

    1. The effects of three daily sessions of inescapable footshock on the sensitivity of rat isolated right atria to the chronotropic effect of norepinephrine, tyramine and Soterenol were studied. 2. Inescapable footshock induces subsensitivity to norepinephrine and tyramine. The maximum response to the partial agonist Soterenol was reduced. 3. In vitro denervation and addition of cocaine prevented the demonstration of inescapable footshock-induced subsensitivity to norepinephrine. 4. It is concluded that repeated inescapable footshock stress reduces the number of atrial beta 1-adrenoceptors and increases the efficiency of the neuronal reuptake process.18473-

  • Subsensitivity To β-adrenoceptor Agonists In Pacemakers Isolated From Senescent Rats
    2015
    Co-Authors: Spadari R.c., Demoraes S
    Abstract:

    1. 1. The effects of aging on the responsiveness of the isolated pacemaker of the rat to the chronotropic effect of norepinephrine, isoproterenol and Soterenol were studied. 2. 2. Pacemakers isolated from senescent rats (22-24 months old) showed subsensitivity to norepinephrine, isoproterenol and Soterenol, when compared with pacemakers isolated from young rats (3-4 months old). The maximum response to the partial agonist Soterenol was reduced. 3. 3. Determination of the pA2 value of metoprolol in pacemakers isolated from senescent and young rats showed that the chronotropic response is mediated by a homogeneous β1-adrenoceptor population. 4. 4. Inhibition of extraneuronal uptake did not potentiate the chronotropic effect of isoproterenol in pacemakers isolated from senescent rats. Addition of cocaine shifted the concentration-effect curve for norepinephrine only 2.2-fold to the left in senescent rats. 5. 5. It is concluded that, during aging, impairment of the extraneuronal and neuronal uptake mechanisms has an important role in the control of chronotropic responsiveness to catecholamines. © 1991.225917921 Information, Control and Communication (INSTICC),Institute for Systems and Technologies ofArunlakshana, Schild, Some quantitative uses of drug antagonists (1959) Br. J. Pharmac. Chemother., 14, pp. 48-58Bassani, de Moraes, Effects of repeated footshock stress on the chronotropic responsiveness of the isolated pacemaker of the rat: role of beta2-adrenoceptors (1988) J. Pharmac. Exp. Ther., 246, pp. 316-321Besse, Furchgott, Dissociation constants and relative efficacies of agonists acting on alpha-adrenergic receptors in rabbit aorta (1976) J. Pharmac. Exp. Ther., 197, pp. 66-78Bryan, Cole, O'Donnell, Wanstall, A study designed to explore the hypothesis that beta1-adrenoceptors are “innervated receptors” and beta2-adrenoceptors are “hormonal receptors” (1981) J. Pharmac. Exp. Ther., 216, pp. 395-400Bückner, Torphy, Costa, Studies on beta-adrenoceptors mediating changes in mechanical events and adenosine 3′-5′-monophosphate level in rat atria (1978) European Journal of Pharmacology, 47, pp. 259-271Callia, de Moraes, Heterogeneity of beta adrenoceptors in right atria isolated from cold-exposed rats (1984) J. Pharmac. Exp. Ther., 230, pp. 450-454Docherty, Changes in adrenoceptor function with age (1988) Vascular Neuroeffector Mechanisms, pp. 281-287. , J.A. Bevan, H. Majewski, R.A. Maxwell, D.F. Story, IRL Press, Oxford, WADocherty, Cardiovascular responses in aging: a review (1990) Pharmac. Rev., 42, pp. 103-124Fan, Banerjee, Age-related reduction of beta-adrenoceptor sensitivity in rat heart occurs by multiple mechanisms (1985) Gerontology, 31, pp. 373-380Fleming, Westfall, de La Lande, Jellett, Log-normal distribution of equi-effective doses of norepinephrine and acetylcholine in several tissues (1972) J. Pharmac. Exp. Ther., 181, pp. 339-345Gey, Burkand, Pletscher, Variation of the norepinephrine metabolism of the rat heart with age (1965) Gerontology, 11, pp. 1-11Guarnieri, Filburn, Zitnik, Roth, Lakatta, Contractile and biochemical correlates of beta-adrenergic stimulation of the aged heart (1980) Am. J. Physiol., 239, pp. H501-H508Juberg, Minneman, Abel, Beta1-and beta2-adrenoceptor binding and functional responses in right and left atria of the rat heart (1985) Naunyn-Schmiedeberg's Arch. Pharmac., 330, pp. 193-202Kenakin, The Schild regression in the process of receptor classification (1982) Can. J. Physiol. Pharmac., 60, pp. 249-265Kenakin, The classification of drugs and drug receptors in isolated tissues (1984) Pharmac. Rev., 36, pp. 165-222Kenakin, Beek, Relative efficacy of prenalterol and pirbuterol: measurement of receptor affinity by alteration of receptor number (1984) J. Pharmac. Exp. Ther., 299, pp. 340-345Kreider, Goldberg, Roberts, Effect of age on adrenergic uptake in rat heart (1984) J. Pharmac. Exp. Ther., 231, pp. 367-372Lakatta, Gerstenblith, Angell, Shock, Weisfeldt, Diminished inotropic response of aged myocardium to catecholamines (1975) Circ. Res., 36, pp. 262-269Lakatta, Gerstenblith, Angell, Shock, Weisfeldt, Prolonged contraction duration in aged myocardium (1975) J. Clin. Invest., 55, pp. 61-68Limas, Comparison of the handling of norepinephrine in the myocardium of adult and old rats (1975) Cardiovasc. Res., 9, pp. 664-668MacGilchrist, Hawksby, Howes, Reid, Rise in plasma noradrenaline with age results from an increase in spillover rate (1989) Gerontology, 35, pp. 7-13Mackay, How should values of pA2 and affinity constants for pharmacological competitive antagonists be estimated? (1978) J. Pharm. Pharmac., 30, pp. 312-313Martinez, Vasques, Messing, Jensen, Liang, McGauth, Age-related changes in catecholamine content of peripheral organs in male and female F344 rats (1981) J. Gerontol., 36, pp. 280-284Montamat, Davies, Physiological response to isoproterenol and coupling of beta-adrenergic receptors in young and elderly human subjects (1989) J. Gerontol., 44, pp. M100-M105O'Donnell, Wanstall, The importance of the choice of the agonist in studies designed to predict beta1:beta2-adrenoceptor selectivity of antagonists from pA2 values of guinea-pig trachea and atria (1979) Naunyn-Schmiedeberg's. Arch. Pharmac., 308, pp. 183-190Pappano, Ontogenetic development of autonomic neuroeffector transmission and transmitter reactivity in embryonic and fetal hearts (1977) Pharmac. Rev., 29, pp. 3-33Roberts, Goldberg, Changes in basic cardiovascular activities during the lifetime of the rat (1976) Exp. Aging Res., 2, pp. 487-517Scarpace, Decreased beta-adrenergic responsiveness during senescence (1986) Fedn Prod. Fedn Am. Socs exp. Biol., 45, pp. 51-54Vargas, Lye, Faragher, Goddard, Moser, Davies, Cardiovascular haemodynamics and the response of vasopressin, aldosterone, plasma renin activity and plasma catecholamines to head-up tilt in young and old healthy subjects (1986) Age Aging, 15, pp. 17-2

  • Subsensitivity To β-adrenoceptor Agonists In Right Atria Isolated From Footshock-stressed Rats
    2015
    Co-Authors: Bassani R.a., Demoraes S
    Abstract:

    1. The effects of three daily sessions of inescapable footshock on the sensitivity of rat isolated right atria to the chronotropic effect of norepinephrine, tyramine and Soterenol were studied. 2. Inescapable footshock induces subsensitivity to norepinephrine and tyramine. The maximum response to the partial agonist Soterenol was reduced. 3. In vitro denervation and addition of cocaine prevented the demonstration of inescapable footshock-induced subsentivity to norepinephrine. 4. It is concluded that repeated inescapable footshock stress reduces the number of atrial β1-adrenoceptors and increases the efficiency of the neuronal reputake process. © 1987.185473477Conseil General de l'Aube',Conseil National de la Recherche Scientifique (CNRS),et al,Grand Troyes,Proto Manufacturing,Region Champagne-ArdenneAprigliano, Hermsmeyer, In vitro denervation of the portal vein and caudal artery of the rat (1976) J. Pharmac. exp. Ther., 198, pp. 568-577Besse, Furchgott, Dissociation constants and relative efficacies of agonists acting on alpha-adrenergic receptors in rabbit aorta (1976) J. Pharmac. exp. Ther., 197, pp. 66-78Bönisch, Fuchs, Graefe, Sodium-dependence of the saturability of carrier-mediated noradrenaline efflux from noradrenergic neurones in the rat vas deferens (1986) Naunyn-Schmiedeberg's Archives of Pharmacology, 332, pp. 131-134Bückner, Torphy, Costa, Studies on β-adrenoceptors mediating changes in mechanical events and adenosine 3′,5′-monophosphate levels. Rat atria (1978) European Journal of Pharmacology, 47, pp. 259-271Callia, De Moraes, Heterogeneity of beta adrenoceptors in right atria isolated from cold-exposed rats (1984) J. Pharmac. exp. Ther., 230, pp. 450-454Chang, Tran, Snyder, Neurotransmitter receptor localization: brain lesion-induced alteration in benzodiazepine, GABA, beta-adrenergic and histamine H1-receptor binding (1980) Brain Research, 190, pp. 95-110Harden, Agonist-induced desensitization of β-adrenergic receptor-linked adenylate cyclase (1983) Pharmac. Rev., 35, pp. 5-32Harri, Melender, Tirri, Changed chronotropic sensitivity to sympathomimetic amines in isolated atri from rats following cold acclimation (1974) Experientia, 30, pp. 1041-1043Hoffman, Fleshler, A relay sequencing device for scrambling grid shock1 (1967) Journal of the Experimental Analysis of Behavior, 5, pp. 329-330Kenakin, Beek, Relative efficacy of prenalterol and pirbuterol: measurement of agonist affinity by alteration of receptor number (1984) J. Pharmac. exp. Ther., 299, pp. 340-345Kendall, Duman, Slopes, Enna, Influence of adrenocorticotropic hormone and yohimbine on antidepressant-induced declines in rat brain neurotransmitter receptor binding and function (1982) J. Pharmac. exp. Ther., 222, pp. 566-571Kvetnanaky, Mikulaj, Adrenal and Urinary Catecholamines in Rats During Adaptation to Repeated Immobilization Stress (1970) Endocrinology, 87, pp. 738-743Snedecor, Cochran, (1967) Statistical Methods, , Iowa State University Press, AmesStone, Effect of stress on norepinephrine-stimulated cyclic AMP formation in brain slices (1978) Pharmacology Biochemistry and Behavior, 8, pp. 583-591Stone, Reduction by stress of norepinephrine-stimulated accumulation of cyclic AMP in rat cerebral cortex (1979) Journal of Neurochemistry, 32, pp. 1335-1337Stone, Subsensitivity to norepineprhine as a link between adaptation to stress and antidepressant therapy: an hypothesis (1979) Res. Commun. Psychol. Psychiat. Behav., 4, pp. 241-255Stone, Adaptation to stress and brain noradrenergic receptors (1983) Neuroscience & Biobehavioral Reviews, 7, pp. 503-509Stone, McCarty, Adaptation to stress: Tyrosine hydroxylase activity and catecholamine release (1983) Neuroscience & Biobehavioral Reviews, 7, pp. 29-34Stone, Platt, Brain Adrenergic receptors and resistance to stress (1982) Brain Research, 237, pp. 405-514Stone, Slucky, Platt, Trullas, Reduction of the cyclic adenosine 3′-5′ monophosphate response to catecholamines in rat brain slices after repeated restraint stress (1985) J. Pharmac. exp. Ther., 233, pp. 382-388Strader, Pickel, Joh, Strohsacker, Shore, Lefkowitz, Caron, Antibodies to the beta-adrenergic receptor: attenuation of catecholamine-sensitive adenylate cyclase and demonstration of postsynaptic receptor localization in brain. (1983) Proceedings of the National Academy of Sciences, 80, pp. 1840-1844Torda, Yamaguchi, Hirata, Kopin, Axelrod, Mepacrine treatment prevents immobilization-induced desensitization of beta-adrenergic receptors in rat hypothalamus and brain stem (1981) Brain Research, 205, pp. 441-444U'Prichard, Kvetnanský, Central and peripheral adrenergic receptor in acute and repeated immobilization stress (1980) Catecholamines and Stress: Recent Advances, pp. 232-299. , E. Usden, R. Kvetnanský, I.J. Kopin, Elsevier North/Holland, New YorkWeiss, Glazer, Pohrecky, Bailey, Schneider, Coping behaviour and stress-induced behavioral depression: studies of the role of brain catecholamines (1977) The Psychobiology of Depressive Disorders: Implications for the Effects of Stress, , R. Depul, Academic Press, New YorkWolfe, Harden, Sporn, Molinoff, Presynaptic modulation of beta adrenergic receptors in rat cerebral cortex after treatment with antidepressants (1978) J. Pharmac. exp. Ther., 207, pp. 446-45

Luiz Carlos Marques Vanderlei - One of the best experts on this subject based on the ideXlab platform.

  • Influencia do ciclo estral e do estresse sobre a sensibilidade as catecolamidas em atrios de ratas
    2017
    Co-Authors: Luiz Carlos Marques Vanderlei
    Abstract:

    Resumo: O objetivo desse trabalho foi analisar as alterações de sensibilidade às catecolaminas em átrios direitos isolados (AD) de ratas submetidas a estresse por choques nas patas e sacrificadas no estro ou diestro. Foram utilizadas ratas Wistar adultas, com ciclo estral regular de 4 dias, submetidas a 3 sessões de choques nas patas no estro, metaestro e diestro ou no diestro, proestro e estro. Cada rata recebeu, durante 30 minutos, 120 choques nas patas (1,0 mA, 1,0 s), a intervalos variáveis de 5 a 25 segundos. Após a última sessão de choques, os animais foram sacrificados e o AD preparado para registro isométrico das contrações espontâneas. Curvas concentração/efeito para noradrenalina (NA), adrenalina (ADR) e Soterenol (SO) foram obtidas sem tratamento farmacológico. Para analisar os mecanismos envolvidos com as alterações de sensibilidade observadas, foram utilizados um ou mais dos seguintes tratamentos farmacológicos: desnervação adrenérgica, inibição dos sistemas de captação extraneuronal e de recaptação neuronal, bem como, bloqueio dos adrenoceptores `alfa´ e muscarínicos. Os dados foram comparados através de análise de variância seguida da aplicação do teste de Scheffé, e pelo teste t de Student. Diferenças foram consideradas significantes ao nível de 5%. AD de ratas, submetidas a choques nas patas e sacrificadas no diestro, apresentaram subsensibilidade à ADR (pD2 = 7,38 `+ ou -´ 0,09 vs. 6,63 `+ ou -´ 0,08), NA (pD2 = 7,67 `+ ou -´ 0,11 vs. 6,95 `+ ou -´ 0,13) e SO (pD2 = 6,80 `+ ou -´ 0,13 vs. 6,36 `+ ou -´ 0,07), quando comparados com os respectivos controles. A inibição do processo de recaptação neuronal cancelou a subsensibilidade à NA (pD2 = 7,88 `+ ou -´ 0,06 vs. 7,73 `+ ou -´ 0,08). Após a realização de tratamento farmacológico completo, AD desses animais continuaram a apresentar subsensibilidade à NA (pD2 = 8,10 `+ ou -´ 0,11 vs. 7,68 `+ ou -´ 0,14), enquanto que a subsensibilidade para a ADR foi cancelada (pD2 = 7,67 `+ ou -´ 0,13 vs. 7,49 `+ ou -´ 0,08). Adição de butoxamina tomou novamente evidente a subsensibilidade à ADR (pD2 = 7,51 `+ ou -´ 0,05 vs. 7,15 `+ ou -´ 0,13). Em AD de ratas estressadas e sacrificadas no estro, somente foi observada subsensibilidade aos efeitos cronotrópicos da adrenalina, após a adição de butoxamina (pD2 = 7,59 `+ ou -´ 0,05 vs. 7,17 `+ ou -´ 0,07). Estes resultados sugerem que, após estresse por choques nas patas, AD de ratas sacrificadas no diestro apresentaram aumento da eficiência do processo de recaptação neuronal, essensibilização dos adrenoceptores `beta 1´ e participação dos adrenoceptores `beta 2´ na resposta cronotrópica às catecolaminas. Durante o estro, os mecanismos adaptativos do controle cronotrópico dos AD pelas catecolaminas não ocorrem, com exceção da participação dos adrenoceptores `beta 2´ na mediação da resposta cronotrópicaAbstract: This study was performed to analyse the alterations in sensitivity to catecholamines in right atria isolated (AD) from rats submitted to footshock stress and sacrificed at estrus or diestrus. Adult Wistar female rats exhibiting regular 4-day estrous cycles were submitted to three footshock sessions at estrus, metestrus and diestrus or at diestrus, proestrus and estrus. Each rat received during 30 min, 120 electricshocks (1. 0 mA, 1.0 s) at variable intervals of 5 to 25 s. After the last session, the animals were sacrificed and its right atria set up for isometric recording of spontaneous beating. Dose-response curves to noradrenaline (NA), adrenaline (ADR) and Soterenol (SQ) were obtained before "in vitro" treatment. To analyse the mechanisms of the alterations in sensitivity one or more of the following "in vitro" treatment were used: sympathetic denervation, inhibition of the extraneuronal uptake and neuronal reuptake and blockade of alpha adrenoceptors and muscarine receptors. Data were compared by using analysis of variance followed by Scheffé test and student t-test. Differences were considered significant at p < 0,05. Right atria from rats submitted to footshock stress and sacrificed at diestrus compared to those from control rats showed subsensitivity to ADR (pD2 = 7.38 ` + or -´ 0,09 vs. 6.63 ` + or -´ 0,08), NA (pD2 = 7.67 ` + or -´ 0.11 vs. 6.95 ` + or -´ 0,13) and SQ (pD2 = 6.80 ` + or -´ 0.13 vs. 6.36 ` + or -´ 0.07). The inhibition of neuronal reuptake canceled the subsensitivity to NA (pD2 = 7.88 ` + or -´ 0.06 vs. 7.73 ` + or -´ 0.08). After complete "in vitro" treatment AD from stressed rats showed subsensitivity to NA (pD2 = 8.10 ` + or -´ 0.11 vs 7.68 ` + or -´ 0.14) however the subsensitivity to ADR was canceled (pD2 = 7.67 ` + or -´ 0.13 vs. 7.49 ` + or -´ 0.08) but returned afier addition of butoxamine (pD2 = 7.51` + or -´ 0.05 vs. 7.15` + or -´ 0.13). Right atria from stressed rats sacrificed at estrus were also subsensitive to ADR afier addition of butoxamine (pD2 = 7.59 ` + or -´ 0.05 vs. 7.17 ` + or -´ 0.07). These results demonstrat that footshock stress, induces an increase in the efficiency of the neuronal reuptake process, desensitization of `beta 1´adrenoceptors and increase in `beta 2´-adrenoceptor-mediated response in right atria from female rats sacrificed at diestrus. During estrus it seems that those adaptive responses of the chronotropic control of the heart by catecholamines do not occur with the exception of the increase in `beta 2´-adrenoceptor-mediated respons

  • Influencia do ciclo estral e do estresse sobre a sensibilidade as catecolamidas em atrios de ratas
    Universidade Estadual de Campinas. Faculdade de Odontologia de Piracicaba, 1996
    Co-Authors: Luiz Carlos Marques Vanderlei
    Abstract:

    O objetivo desse trabalho foi analisar as alterações de sensibilidade às catecolaminas em átrios direitos isolados (AD) de ratas submetidas a estresse por choques nas patas e sacrificadas no estro ou diestro. Foram utilizadas ratas Wistar adultas, com ciclo estral regular de 4 dias, submetidas a 3 sessões de choques nas patas no estro, metaestro e diestro ou no diestro, proestro e estro. Cada rata recebeu, durante 30 minutos, 120 choques nas patas (1,0 mA, 1,0 s), a intervalos variáveis de 5 a 25 segundos. Após a última sessão de choques, os animais foram sacrificados e o AD preparado para registro isométrico das contrações espontâneas. Curvas concentração/efeito para noradrenalina (NA), adrenalina (ADR) e Soterenol (SO) foram obtidas sem tratamento farmacológico. Para analisar os mecanismos envolvidos com as alterações de sensibilidade observadas, foram utilizados um ou mais dos seguintes tratamentos farmacológicos: desnervação adrenérgica, inibição dos sistemas de captação extraneuronal e de recaptação neuronal, bem como, bloqueio dos adrenoceptores `alfa´ e muscarínicos. Os dados foram comparados através de análise de variância seguida da aplicação do teste de Scheffé, e pelo teste t de Student. Diferenças foram consideradas significantes ao nível de 5%. AD de ratas, submetidas a choques nas patas e sacrificadas no diestro, apresentaram subsensibilidade à ADR (pD2 = 7,38 `+ ou -´ 0,09 vs. 6,63 `+ ou -´ 0,08), NA (pD2 = 7,67 `+ ou -´ 0,11 vs. 6,95 `+ ou -´ 0,13) e SO (pD2 = 6,80 `+ ou -´ 0,13 vs. 6,36 `+ ou -´ 0,07), quando comparados com os respectivos controles. A inibição do processo de recaptação neuronal cancelou a subsensibilidade à NA (pD2 = 7,88 `+ ou -´ 0,06 vs. 7,73 `+ ou -´ 0,08). Após a realização de tratamento farmacológico completo, AD desses animais continuaram a apresentar subsensibilidade à NA (pD2 = 8,10 `+ ou -´ 0,11 vs. 7,68 `+ ou -´ 0,14), enquanto que a subsensibilidade para a ADR foi cancelada (pD2 = 7,67 `+ ou -´ 0,13 vs. 7,49 `+ ou -´ 0,08). Adição de butoxamina tomou novamente evidente a subsensibilidade à ADR (pD2 = 7,51 `+ ou -´ 0,05 vs. 7,15 `+ ou -´ 0,13). Em AD de ratas estressadas e sacrificadas no estro, somente foi observada subsensibilidade aos efeitos cronotrópicos da adrenalina, após a adição de butoxamina (pD2 = 7,59 `+ ou -´ 0,05 vs. 7,17 `+ ou -´ 0,07). Estes resultados sugerem que, após estresse por choques nas patas, AD de ratas sacrificadas no diestro apresentaram aumento da eficiência do processo de recaptação neuronal, essensibilização dos adrenoceptores `beta 1´ e participação dos adrenoceptores `beta 2´ na resposta cronotrópica às catecolaminas. Durante o estro, os mecanismos adaptativos do controle cronotrópico dos AD pelas catecolaminas não ocorrem, com exceção da participação dos adrenoceptores `beta 2´ na mediação da resposta cronotrópicaThis study was performed to analyse the alterations in sensitivity to catecholamines in right atria isolated (AD) from rats submitted to footshock stress and sacrificed at estrus or diestrus. Adult Wistar female rats exhibiting regular 4-day estrous cycles were submitted to three footshock sessions at estrus, metestrus and diestrus or at diestrus, proestrus and estrus. Each rat received during 30 min, 120 electric shocks (1. 0 mA, 1.0 s) at variable intervals of 5 to 25 s. After the last session, the animals were sacrificed and its right atria set up for isometric recording of spontaneous beating. Dose-response curves to noradrenaline (NA), adrenaline (ADR) and Soterenol (SQ) were obtained before "in vitro" treatment. To analyse the mechanisms of the alterations in sensitivity one or more of the following "in vitro" treatment were used: sympathetic denervation, inhibition of the extraneuronal uptake and neuronal reuptake and blockade of alpha adrenoceptors and muscarine receptors. Data were compared by using analysis of variance followed by Scheffé test and student t-test. Differences were considered significant at p < 0,05. Right atria from rats submitted to footshock stress and sacrificed at diestrus compared to those from control rats showed subsensitivity to ADR (pD2 = 7.38 ` + or -´ 0,09 vs. 6.63 ` + or -´ 0,08), NA (pD2 = 7.67 ` + or -´ 0.11 vs. 6.95 ` + or -´ 0,13) and SQ (pD2 = 6.80 ` + or -´ 0.13 vs. 6.36 ` + or -´ 0.07). The inhibition of neuronal reuptake canceled the subsensitivity to NA (pD2 = 7.88 ` + or -´ 0.06 vs. 7.73 ` + or -´ 0.08). After complete "in vitro" treatment AD from stressed rats showed subsensitivity to NA (pD2 = 8.10 ` + or -´ 0.11 vs 7.68 ` + or -´ 0.14) however the subsensitivity to ADR was canceled (pD2 = 7.67 ` + or -´ 0.13 vs. 7.49 ` + or -´ 0.08) but returned afier addition of butoxamine (pD2 = 7.51` + or -´ 0.05 vs. 7.15` + or -´ 0.13). Right atria from stressed rats sacrificed at estrus were also subsensitive to ADR afier addition of butoxamine (pD2 = 7.59 ` + or -´ 0.05 vs. 7.17 ` + or -´ 0.07). These results demonstrat that footshock stress, induces an increase in the efficiency of the neuronal reuptake process, desensitization of `beta 1´adrenoceptors and increase in `beta 2´-adrenoceptor-mediated response in right atria from female rats sacrificed at diestrus. During estrus it seems that those adaptive responses of the chronotropic control of the heart by catecholamines do not occur with the exception of the increase in `beta 2´-adrenoceptor-mediated respons

Vanderlei, Luiz Carlos Marques - One of the best experts on this subject based on the ideXlab platform.

  • Influencia do ciclo estral e do estresse sobre a sensibilidade as catecolamidas em atrios de ratas
    [s.n.], 2018
    Co-Authors: Vanderlei, Luiz Carlos Marques
    Abstract:

    Orientadores: Regina Celia Spadari-Bratfisch, Maria Cecilia Ferraz de Arruda VeigaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de PiracicabaResumo: O objetivo desse trabalho foi analisar as alterações de sensibilidade às catecolaminas em átrios direitos isolados (AD) de ratas submetidas a estresse por choques nas patas e sacrificadas no estro ou diestro. Foram utilizadas ratas Wistar adultas, com ciclo estral regular de 4 dias, submetidas a 3 sessões de choques nas patas no estro, metaestro e diestro ou no diestro, proestro e estro. Cada rata recebeu, durante 30 minutos, 120 choques nas patas (1,0 mA, 1,0 s), a intervalos variáveis de 5 a 25 segundos. Após a última sessão de choques, os animais foram sacrificados e o AD preparado para registro isométrico das contrações espontâneas. Curvas concentração/efeito para noradrenalina (NA), adrenalina (ADR) e Soterenol (SO) foram obtidas sem tratamento farmacológico. Para analisar os mecanismos envolvidos com as alterações de sensibilidade observadas, foram utilizados um ou mais dos seguintes tratamentos farmacológicos: desnervação adrenérgica, inibição dos sistemas de captação extraneuronal e de recaptação neuronal, bem como, bloqueio dos adrenoceptores 'alfa' e muscarínicos. Os dados foram comparados através de análise de variância seguida da aplicação do teste de Scheffé, e pelo teste t de Student. Diferenças foram consideradas significantes ao nível de 5%. AD de ratas, submetidas a choques nas patas e sacrificadas no diestro, apresentaram subsensibilidade à ADR (pD2 = 7,38 '+ ou -' 0,09 vs. 6,63 '+ ou -' 0,08), NA (pD2 = 7,67 '+ ou -' 0,11 vs. 6,95 '+ ou -' 0,13) e SO (pD2 = 6,80 '+ ou -' 0,13 vs. 6,36 '+ ou -' 0,07), quando comparados com os respectivos controles. A inibição do processo de recaptação neuronal cancelou a subsensibilidade à NA (pD2 = 7,88 '+ ou -' 0,06 vs. 7,73 '+ ou -' 0,08). Após a realização de tratamento farmacológico completo, AD desses animais continuaram a apresentar subsensibilidade à NA (pD2 = 8,10 '+ ou -' 0,11 vs. 7,68 '+ ou -' 0,14), enquanto que a subsensibilidade para a ADR foi cancelada (pD2 = 7,67 '+ ou -' 0,13 vs. 7,49 '+ ou -' 0,08). Adição de butoxamina tomou novamente evidente a subsensibilidade à ADR (pD2 = 7,51 '+ ou -' 0,05 vs. 7,15 '+ ou -' 0,13). Em AD de ratas estressadas e sacrificadas no estro, somente foi observada subsensibilidade aos efeitos cronotrópicos da adrenalina, após a adição de butoxamina (pD2 = 7,59 '+ ou -' 0,05 vs. 7,17 '+ ou -' 0,07). Estes resultados sugerem que, após estresse por choques nas patas, AD de ratas sacrificadas no diestro apresentaram aumento da eficiência do processo de recaptação neuronal, essensibilização dos adrenoceptores 'beta 1' e participação dos adrenoceptores 'beta 2' na resposta cronotrópica às catecolaminas. Durante o estro, os mecanismos adaptativos do controle cronotrópico dos AD pelas catecolaminas não ocorrem, com exceção da participação dos adrenoceptores 'beta 2' na mediação da resposta cronotrópicaAbstract: This study was performed to analyse the alterations in sensitivity to catecholamines in right atria isolated (AD) from rats submitted to footshock stress and sacrificed at estrus or diestrus. Adult Wistar female rats exhibiting regular 4-day estrous cycles were submitted to three footshock sessions at estrus, metestrus and diestrus or at diestrus, proestrus and estrus. Each rat received during 30 min, 120 electric shocks (1. 0 mA, 1.0 s) at variable intervals of 5 to 25 s. After the last session, the animals were sacrificed and its right atria set up for isometric recording of spontaneous beating. Dose-response curves to noradrenaline (NA), adrenaline (ADR) and Soterenol (SQ) were obtained before "in vitro" treatment. To analyse the mechanisms of the alterations in sensitivity one or more of the following "in vitro" treatment were used: sympathetic denervation, inhibition of the extraneuronal uptake and neuronal reuptake and blockade of alpha adrenoceptors and muscarine receptors. Data were compared by using analysis of variance followed by Scheffé test and student t-test. Differences were considered significant at p < 0,05. Right atria from rats submitted to footshock stress and sacrificed at diestrus compared to those from control rats showed subsensitivity to ADR (pD2 = 7.38 ' + or -' 0,09 vs. 6.63 ' + or -' 0,08), NA (pD2 = 7.67 ' + or -' 0.11 vs. 6.95 ' + or -' 0,13) and SQ (pD2 = 6.80 ' + or -' 0.13 vs. 6.36 ' + or -' 0.07). The inhibition of neuronal reuptake canceled the subsensitivity to NA (pD2 = 7.88 ' + or -' 0.06 vs. 7.73 ' + or -' 0.08). After complete "in vitro" treatment AD from stressed rats showed subsensitivity to NA (pD2 = 8.10 ' + or -' 0.11 vs 7.68 ' + or -' 0.14) however the subsensitivity to ADR was canceled (pD2 = 7.67 ' + or -' 0.13 vs. 7.49 ' + or -' 0.08) but returned afier addition of butoxamine (pD2 = 7.51' + or -' 0.05 vs. 7.15' + or -' 0.13). Right atria from stressed rats sacrificed at estrus were also subsensitive to ADR afier addition of butoxamine (pD2 = 7.59 ' + or -' 0.05 vs. 7.17 ' + or -' 0.07). These results demonstrat that footshock stress, induces an increase in the efficiency of the neuronal reuptake process, desensitization of 'beta 1'adrenoceptors and increase in 'beta 2'-adrenoceptor-mediated response in right atria from female rats sacrificed at diestrus. During estrus it seems that those adaptive responses of the chronotropic control of the heart by catecholamines do not occur with the exception of the increase in 'beta 2'-adrenoceptor-mediated responseDoutoradoFarmacologiaDoutor em Odontologi

Bassani R A - One of the best experts on this subject based on the ideXlab platform.

  • Subsensitivity To Beta-adrenoceptor Agonists In Right Atria Isolated From Footshock-stressed Rats.
    2015
    Co-Authors: Bassani R A, Demoraes S
    Abstract:

    1. The effects of three daily sessions of inescapable footshock on the sensitivity of rat isolated right atria to the chronotropic effect of norepinephrine, tyramine and Soterenol were studied. 2. Inescapable footshock induces subsensitivity to norepinephrine and tyramine. The maximum response to the partial agonist Soterenol was reduced. 3. In vitro denervation and addition of cocaine prevented the demonstration of inescapable footshock-induced subsensitivity to norepinephrine. 4. It is concluded that repeated inescapable footshock stress reduces the number of atrial beta 1-adrenoceptors and increases the efficiency of the neuronal reuptake process.18473-

  • Effects Of Escapable And Inescapable Foot-shock On Rat Atrial Beta-adrenoceptors.
    2015
    Co-Authors: Bassani R A, Bassani J W
    Abstract:

    The chronotropic responsiveness to norepinephrine (NE) and isoproterenol (ISO) was determined in right atria isolated from rats submitted to repeated escapable or inescapable foot-shock. Significant postjunctional supersensitivity to ISO, but not to NE, was observed in both groups. No significant change in the pA2 value of metoprolol (a selective beta 1-adrenoceptor antagonist) was detected. However, a decrease of the maximum response to Soterenol, a partial agonist at beta 1-adrenoceptors, occurred only after inescapable foot-shock. The enhanced sensitivity to ISO was abolished by butoxamine (a selective beta 2-adrenoceptor antagonist) and accompanied by a marked increase in the pA2 value of this antagonist. We conclude that the ability to control the shock prevented the down-regulation of the pacemaker beta 1-adrenoceptors but not the increased participation of beta 2-adrenoceptors in the response of the rat sinoatrial node to catecholamines after repeated foot-shock.44869-7

Rc Spadari - One of the best experts on this subject based on the ideXlab platform.

  • SUBSENSITIVITY TO BETA-ADRENOCEPTOR AGONISTS IN PACEMAKERS ISOLATED FROM SENESCENT RATS
    'Elsevier BV', 2015
    Co-Authors: Rc Spadari, Demoraes S
    Abstract:

    1. The effects of aging on the responsiveness of the isolated pacemaker of the rat to the chronotropic effect of norepinephrine, isoproterenol and Soterenol were studied. 2. Pacemakers isolated from senescent rats (22-24 months old) showed subsensitivity to norepinephrine, isoproterenol and Soterenol, when compared with pacemakers isolated from young rats (3-4 months old). The maximum response to the partial agonist Soterenol was reduced. 3. Determination of the pA2 value of metoprolol in pacemakers isolated from senescent and young rats showed that the chronotropic response is mediated by a homogeneous beta-1-adrenoceptor population. 4. Inhibition of extraneuronal uptake did not potentiate the chronotropic effect of isoproterenol in pacemakers isolated from senescent rats. Addition of cocaine shifted the concentration-effect curve for norepinephrine only 2.2-fold to the left in senescent rats. 5. It is concluded that, during aging, impairment of the extraneuronal and neuronal uptake mechanisms has an important role in the control of chronotropic responsiveness to catecholamines.22591792