No presente trabalho investigamos em ratos hipertensos espontâneos (SHR) e seus controles normotensos (WKY) os efeitos do treinamento físico sobre a atividade simpática a diferentes territórios, bem como os efeitos da remoção seletiva dos baroreceptores arteriais sobre a atividade simpática. SHR e WKY foram submetidos à desnervação sino-aórtica (SAD) ou cirurgia fictícia (SHAM) e alocados aos grupos T (50-60% da capacidade máxima, 1 hora/dia, 5 dias/semana) ou mantidos sedentários (S) por 3 meses.Nossos dados demonstraram que as adaptações induzidas pelo T no simpático periférico são tecido-específicos e dependem da linhagem experimental: redução do simpático ao coração e rins de WKY e SHR, com redução da atividade simpática ao músculo esquelético nos WKY treinados, mas aumentado nos SHR treinados, os quais apresentam simultaneamente extenso remodelamento vascular. Nossos dados demonstraram ainda, que as adaptações do simpático induzidas pelo T dependem da integridade dos baroreceptores arteriais. / In the present study we investigate in spontaneous hypertensive rats (SHR) and their normotensive controls (WKY) the effects of exercise training on sympathetic activity to different territories and the effects of the selective removal of arterial baroreceptors on sympathetic activity. SHR and WKY were subjected to sinoaortic denervation (SAD) or sham surgery (SHAM) and submitted to T (50-60% of maximum capacity, 1 hour / day, 5 days/week) or kept sedentary (S) for 3 months.Our data demonstrated that T-induced changes in peripheral sympathetic innervations are tissue-specific and depend on the experimental strain: reduced sympathetic to the heart and kidneys in WKY and SHR strains, and reduced sympathetic activity to the skeletal muscles in the trained WKY, but increased sympathetic activity in the trained SHR, which showed a simultaneous extensive vascular remodeling after training. Our results also demonstrated that training-induced sympathetic adaptations depend on the integrity of the arterial baroreceptors.

Cardiovascular diseases form one of the most dangerous events that affect human life. They are usually the result of high blood pressure. Thus controlling blood pressure within patient specific healthy limits is a goal that we must target. There are two control loops for blood haemostasis inside the body either long term or short term. Baroreceptors control the short term blood pressure regulation. They are nerve endings that exist in certain locations within the blood vessel walls and they report blood pressure into the brain and the central nervous system. However the basics of their function are not yet known. We propose here that the baroreceptors work by converting circumferential and axial pressure into a stress into their respective direction and they start to send nerve signals based on a threshold of strain energy of the location they are embedded in. Thus baroreceptors A fibre is highly likely to exist in the stiffer adventitia, while the media will contain C fibres. This explains the reason behind having identical fibres with different threshold. We were able to arrive to this solution by getting a relationship between stress–strain relationship for the whole wall and for the arterial vessels. These findings are quiet significant as they allow a method to identify different stress in the arterial wall layers using whole wall experimental data and also as they were able to differentiate between different fibres based on their locations inside the arterial wall. A complete modelling of the baroreceptors function might lead to the formation of biosynthetic material that could interact with the body on the cellular level, so as to give humans the mean to the control of short term blood regulation thus preventing hypertension and its accompanying diseases such as atherosclerosis.

This study compared whether activation of muscle ergoreceptor afferents caused by isometric muscle contraction, activation of baroreceptor afferents induced by i.v. infusion of phenylephrine, or baroreceptor afferent inactivation, caused by carotid artery occlusion, elicit similar patterns of c-Fos induction in brainstem areas. Adult cats were anesthetized with α-chloralose, and in each case, the experimental intervention caused an increase in the arterial blood pressure. There were two sets of control experiments: in both, animals underwent the same surgical procedures but then either remained at rest for the entire study, or the tibial nerve was stimulated, as in the contraction group, following muscle paralysis with tubocurarine. Following the procedures, animals rested for 90 min to allow neuronal expression of c-Fos. Control cats showed very little c-Fos immunoreactivity (c-Fos-ir) in the brainstem. Muscle contraction induced c-Fos-ir expression mainly in the nucleus tractus solitarius, lateral reticular nucleus, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, spinal trigeminal tract and in a lateral region of the periaqueductal grey (P 0.5-1.0). The majority of the c-Fos-ir was found in brainstem areas contralateral to the contracted muscle. In addition, muscle contraction induced c-Fos-ir in the dorsal horns of spinal segments L6-S1 on the ipsilateral side of the spinal cord. Phenylephrine infusion caused c-Fos-ir expression in the nucleus tractus solitarius, spinal trigeminal tract, solitary tract, and dorsal motor nucleus of the vagus. No c-Fos-ir was apparent in the periaqueductal grey. Carotid occlusions induced c-Fos-ir expression in the area postrema, nucleus tractus solitarius, solitary tract, and spinal trigeminal tract. Expression was bilateral. Areas that exhibited c-Fos-ir correspond to sites previously reported to release various neuropeptides in response to muscle contraction or carotid occlusions. These results indicate that the exercise pressor reflex and baroreflex activate similar, but not completely identical, sites in the brainstem.

Substance P (SP) is associated with metabo- and mechanoreceptor afferent fibers ('ergoreceptors') in skeletal muscle as well as the afferent fibers from carotid sinus baroreceptors. Afferent activity from each of these are at least partially integrated in the nucleus tractus solitarius (NTS). The purpose of this study was to determine whether SP was released from the NTS during acute reflex-induced changes in blood pressure caused by stimulating these receptors. Both the muscle pressor response and the baroreflex were studied in adult cats anaesthetized with α-chloralose. SP antibody-coated microprobes were used to measure the possible release of SP from the NTS. The muscle pressor response caused a release of immunoreactive SP-like substances (irSP) from the rostral medial NTS, as well as the dorsal motor nucleus (DMV) and lateral tegmental field (FTL). This release was not dependent on intact afferent input from the carotid sinus nerve, but was a function of activation of muscle ergoreceptors, since no irSP was released in response to stimulation of the motor nerves after the muscle was paralyzed. There was no detectable release of irSP from the mNTS during carotid artery occlusions (baroreceptor unloading). Baroreceptor activation, induced by the i.v. injection of the vasoconstrictor, phenylephrine, did not cause the release of irSP from the mNTS above resting baseline levels. These data suggest that SP is involved with the mediation of the afferent signal from muscle ergoreceptor fibers in the medial NTS. SP is not involved with the mediation of baroreceptor afferent signaling in the medial NTS. The release of SP in response to ergoreceptors activation may function to excite an inhibitory pathway which inhibits baroreflex signals that would tend to reduce the blood pressure and heart rate during the muscle pressor response.

Vagus nerve stimulation (VNS) currently treats patients with drug-resistant epilepsy, depression, and heart failure. The mild intensities used in chronic VNS suggest that primary visceral afferents and central nervous system activation are involved. Here, we measured the activity of neurons in the nucleus of the solitary tract (NTS) in anesthetized rats using clinically styled VNS. Our chief findings indicate that VNS at threshold bradycardic intensity activated NTS neuron discharge in one-third of NTS neurons. This VNS directly activated only myelinated vagal afferents projecting to second-order NTS neurons. Most VNS-induced activity in NTS, however, was unsynchronized to vagal stimuli. Thus, VNS activated unsynchronized activity in NTS neurons that were second order to vagal afferent C-fibers as well as higher-order NTS neurons only polysynaptically activated by the vagus. Overall, cardiovascular-sensitive and -insen-sitive NTS neurons were similarly activated by VNS: 3/4 neurons with monosynaptic vagal A-fiber afferents, 6/42 neurons with monosynaptic vagal C-fiber afferents, and 16/21 polysynaptic NTS neurons. Provocatively, vagal A-fibers indirectly activated C-fiber neurons during VNS. Elevated spontaneous spiking was quantitatively much higher than synchronized activity and extended well into the periods of nonstimulation. Surprisingly, many polysynaptic NTS neurons responded to half the bradycardic intensity used in clinical studies, indicating that a subset of myelinated vagal afferents is sufficient to evoke VNS indirect activation. Our study uncovered a myelinated vagal afferent drive that indirectly activates NTS neurons and thus central pathways beyond NTS and support reconsideration of brain contributions of vagal afferents underpinning of therapeutic impacts. NEW & NOTEWORTHY Acute vagus nerve stimulation elevated activity in neurons located in the medial nucleus of the solitary tract. Such stimuli directly activated only myelinated vagal afferents but indirectly activated a subpopulation of second- and higher-order neurons, suggesting that afferent mechanisms and central neuron activation may be responsible for vagus nerve stimulation efficacy.

Prolonged exposure to microgravity is known to invoke physiological changes which predispose individuals to orthostatic intolerance upon readaptation to the earth's gravitational field. Attenuated baroreflex responsiveness has been implicated in contributing to this inability to withstand orthostatic stress. To test this hypothesis, eight individuals were exposed to 15 days of simulated microgravity exposure using the 6° head-down bed rest model. Prior to, and after the simulated microgravity exposure, the following were assessed: a) aortic baroreflex function; b) carotid baroreflex function; c) cardiopulmonary baroreflex function; and d) the degree of interaction between the cardiopulmonary and carotid baroreflexes.

Reductions in baroreflex responsiveness have been thought to increase the prevalence of orthostatic hypotension in endurance trained athletes. To test this hypothesis, cardiovascular responses to orthostatic stress, cardiopulmonary and carotid baroreflex responsiveness, and the effect of cardiopulmonary receptor deactivation on carotid baroreflex responses were examined in 24 men categorized by maximal aerobic power (V02max) into one of three groups: high fit (HF, V0-2max=67.0±1.9 ml•kg^-1•min^-1), moderately fit (MF, V0-2max=50.9±1.4 ml•kg^-1•min^-1), and low fit (LF, V0-2max=38.9±1.5 ml•kg^-1•min^-1). Orthostatic stress was induced using lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 torr. Cardiopulmonary baroreflex responsiveness was assessed as the slope of the relationship between forearm vascular resistance (FVR, strain gauge plethysmography) and central venous pressure (CVP, dependent arm technigue) during LBNP<-35 torr. Carotid baroreflex responsiveness was assessed as the change in heart rate (HR, electrocardiography) or mean arterial pressure (MAP, radial artery catheter) elicited by 600 msec pulses of neck pressure and neck suction (NP/NS) from +40 to -70 torr. Pressures were applied using a lead collar wrapped about the subjects' necks during held expiration. Stimulus response data were fit to a logistic model and the parameters describing the curve were compared using two-factor ANOVA. The reductions CVP, mean (MAP), systolic, and pulse pressures during LBNP were similar between groups (P<0.05). However, diastolic blood pressure increased during LBNP m all but the HF group. (P<0.05). The slope of the FVR/CVP relationship did not differ between groups, nor did the form of the carotid-cardiac baroreflex stimulus response curve change during LBNP. changes in HR elicited with NP/NS were not different between groups (£>0.05). The range of the MAP stimulus response curve, however, was significantly less in the HP group compared to either the MP or LF group (£<0.05). These data imply that carotid baroreflex control of HR is unaltered by endurance exercise training, but carotid baroreflex control of blood pressure is impaired significantly, predisposing athletes to faintness.

Chen Fei. / "October 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 189-210). Also available on the Internet.

Submitted by Alison Vanceto (alison-vanceto@hotmail.com) on 2017-02-01T10:40:13Z No. of bitstreams: 1 TeseLAZ.pdf: 5426859 bytes, checksum: 033582b6221f018d86ae920b42835b76 (MD5) / Approved for entry into archive by Camila Passos (camilapassos@ufscar.br) on 2017-02-08T12:03:04Z (GMT) No. of bitstreams: 1 TeseLAZ.pdf: 5426859 bytes, checksum: 033582b6221f018d86ae920b42835b76 (MD5) / Approved for entry into archive by Camila Passos (camilapassos@ufscar.br) on 2017-02-08T12:05:28Z (GMT) No. of bitstreams: 1 TeseLAZ.pdf: 5426859 bytes, checksum: 033582b6221f018d86ae920b42835b76 (MD5) / Made available in DSpace on 2017-02-08T12:05:35Z (GMT). No. of bitstreams: 1 TeseLAZ.pdf: 5426859 bytes, checksum: 033582b6221f018d86ae920b42835b76 (MD5) Previous issue date: 2016-10-26 / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / For adequate blood supply to match metabolic demand, vertebrates regulate blood pressure (BP) in order to maintain adequate perfusion of target organs avoiding ischemia and tissue damage like edema. Effective short-term BP regulation in anuran amphibians occurs through adjustments in heart rate (HR), peripheral vascular resistance, and changing pulsatile frequency of lymph hearts. In addition, pulmonary ventilation in anurans is directly linked to blood volume homeostasis by facilitating lymph fluid movement back into the cardiovascular system which takes place by changing pressure and volume within anurans' lymphatic sacs. It is apparent that an interaction between baroreflex regulation and breathing control exists in anuran amphibians. In the present study I used pharmacological methods (phenylephrine and sodium nitroprusside; infusion ramp and in bolus methods) to investigate baroreflex sensitivity at different temperatures in the cururu toad Rhinella schneideri. I evaluated the degree to which arterial baroreflex plays a role in pulmonary ventilation in the cururu toad. Baroreflex regulation in the toad R. schneideri was temperature dependent and influenced the toad’s ventilation. Hypotension and hypertension resulted in increases and decreases in HR, respectively, as well as increases and decreases in pulmonary ventilation mainly through adjustments in breathing frequency. In contrast to data from the literature, anuran amphibians seem to defend lower BP events primarily rather than hypertension independent of temperature. Anurans exhibit higher rates of transcapillary fluid filtration which means during hypertension fluid filtration is increased and excess interstitial fluid formation will be reclaimed by an efficient lymphatic system. Therefore, besides pulmonary ventilation's role in matching O2 delivery to demand (e.g. temperatures) in anurans, it also plays a role in BP regulation possibly owing to an interaction between baroreflex control and respiratory areas in the brain. / Para um adequado suprimento sanguíneo de modo a atender as diferentes demandas metabólicas, os vertebrados regulam a pressão arterial (PA) mantendo adequada perfusão dos órgãos evitando assim eventos isquêmicos ou outros danos teciduais, como edema. O controle efetivo da PA a curto prazo em anfíbios anuros se dá por ajustes da frequência cardíaca (FC), resistência vascular periférica e também por ajustes da frequência de pulsação dos corações linfáticos. Além disso, a ventilação pulmonar nos anuros está diretamente associada à homeostase do volume sanguíneo por meio da facilitação do transporte de fluído linfático de volta ao sistema cardiovascular, que se dá por meio da alteração de pressão e volume dos sacos linfáticos. Isso parece sugerir a existência de uma possível interação entre a regulação barorreflexa e o controle da respiração nos anfíbios anuros, como já observado para os mamíferos. No presente estudo utilizamos de um método farmacológico (fenilefrina e nitroprussiato de sódio: infusão em rampa e injeção in bolus) para investigar a sensibilidade barorreflexa em diferentes temperaturas no sapo cururu Rhinella schneideri. Também avaliamos o papel do barorreflexo arterial na modulação da ventilação pulmonar nesta mesma espécie. A regulação barorreflexa no sapo R. schneideri apresentou dependência térmica, além de afetar consideravelmente a ventilação dos sapos. A hipotensão e hipertensão resultaram em aumentos e reduções da FC, respectivamente, bem como na ventilação pulmonar, que se deu prioritariamente por meio de ajustes na frequência respiratória. Ao contrário dos dados da literatura, os anfíbios anuros parecem defender prioritariamente eventos de hipotensão ao invés da hipertensão, independente da temperatura testada. É importante salientar que os anuros apresentam alta taxa de filtração transcapilar, e que durante eventos de PA elevada, um aumento na formação de fluido transcapilar pulmonar seria recrutado por um eficiente sistema linfático, característico dos anuros. Portanto, apesar da função da ventilação pulmonar em corresponder à disponibilidade de O2 em diferentes demandas metabólicas (e.g. temperatura), também parece apresentar participação na regulação da PA, possivelmente devido a uma interação entre o barorreflexo e as áreas respiratórias no sistema nervoso central.