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High salt intake increases blood pressure, and dietary salt intake has been clearly demonstrated to be associated with hypertension incidence. Japanese people consume higher amounts of salt than Westerners. It has been reported that miso soup was one of the major sources of daily salt intake in Japanese people. Adding salt is indispensable to make miso, and therefore, in some cases, refraining from miso soup is recommended to reduce dietary salt intake. However, recent studies using salt-sensitive hypertensive models have revealed that miso lessens the effects of salt on blood pressure. In other word, the intake of miso dose not increase the blood pressure compared to the equivalent intake of salt. In addition, many clinical observational studies have demonstrated the absence of a relationship between the frequency of miso soup intake and blood pressure levels or hypertension incidence. The mechanism of this phenomenon seen in the subjects with miso soup intake has not been fully elucidated yet. However, in basic studies, it was found that the ingredients of miso attenuate sympathetic nerve activity, resulting in lowered blood pressure and heart rate. Therefore, this review focused on the differences between the effects of miso intake and those of the equivalent salt intake on sympathetic nerve activity, blood pressure, and heart rate.
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Humanos , Pressão Sanguínea , Fisiologia , Frequência Cardíaca , Fisiologia , Alimentos de Soja , Sistema Nervoso Simpático , FisiologiaRESUMO
It is well known that elderly patients with heart failure have low tolerance to exercise. Heart disease increases the cardiac load and causes severe arrhythmias due to an increase in the afferent stimuli from peripheral tissues such as skeletal muscle and from the sympathetic nervous system. Managing risk during exercise from the peripheral factors is essential to improve the quality of life of this patient population. Previous research involved utilizing high-intensity exercise and invasive methods, but it is necessary to perform at a safe intensity to evaluate the tolerance to exercise during rehabilitation. Therefore, the purpose of this study was to assess the changes in ventilatory and circulatory indices caused by venous ischemia after moderate-intensity exercise. The participants comprised ten healthy men randomly assigned to either a venous blood flow shut off task (task1) or the venous blood flow task (task 2). After 2 days or more the tasks were switched. The protocol was performed using a moderate intensity of rest for a while and performing a 4-min cycling exercise at 200 mmHg while occluding venous outflow of the left leg. Immediately after the termination, both groups took 5 min of rest. Task 1 involved occlusion of the venous outflow using 90 mmHg applied to the left thigh. The result showed that in normal subjects, shutting off the venous blood flow did not change the ventilatory response after moderate-intensity exercise but it changed the circulation index.
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Chronic intermittent hypobaric hypoxia (CIHH) is known to have an anti-hypertensive effect, which might be related to modulation of the baroreflex in rats with renal vascular hypertension (RVH). In this study, RVH was induced by the 2-kidney-1-clip method (2K1C) in adult male Sprague-Dawley rats. The rats were then treated with hypobaric hypoxia simulating 5000 m altitude for 6 h/day for 28 days. The arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were measured before and after microinjection of L-arginine into the nucleus tractus solitarii (NTS) in anesthetized rats. Evoked excitatory postsynaptic currents (eEPSCs) and spontaneous EPSCs (sEPSCs) were recorded in anterogradely-labeled NTS neurons receiving baroreceptor afferents. We measured the protein expression of neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS) in the NTS. The results showed that the ABP in RVH rats was significantly lower after CIHH treatment. The inhibition of ABP, HR, and RSNA induced by L-arginine was less in RVH rats than in sham rats, and greater in the CIHH-treated RVH rats than the untreated RVH rats. The eEPSC amplitude in NTS neurons receiving baroreceptor afferents was lower in the RVH rats than in the sham rats and recovered after CIHH. The protein expression of nNOS and eNOS in the NTS was lower in the RVH rats than in the sham rats and this decrease was reversed by CIHH. In short, CIHH treatment decreases ABP in RVH rats via up-regulating NOS expression in the NTS.
Assuntos
Animais , Masculino , Barorreflexo , Fisiologia , Pressão Sanguínea , Hipertensão , Metabolismo , Hipóxia , Rim , Metabolismo , Óxido Nítrico Sintase Tipo I , Metabolismo , Ratos Sprague-Dawley , Núcleo Solitário , MetabolismoRESUMO
The rostral ventrolateral medulla (RVLM) is a key region in cardiovascular regulation. It has been demonstrated that cholinergic synaptic transmission in the RVLM is enhanced in hypertensive rats. Angiotensin-converting enzyme 2 (ACE2) in the brain plays beneficial roles in cardiovascular function in hypertension. The purpose of this study was to determine the effect of ACE2 overexpression in the RVLM on cholinergic synaptic transmission in spontaneously hypertensive rats (SHRs). Four weeks after injecting lentiviral particles containing enhanced green fluorescent protein and ACE2 bilaterally into the RVLM, the blood pressure and heart rate were notably decreased. ACE2 overexpression significantly reduced the concentration of acetylcholine in microdialysis fluid from the RVLM and blunted the decrease in blood pressure evoked by bilateral injection of atropine into the RVLM in SHRs. In conclusion, we suggest that ACE2 overexpression in the RVLM attenuates the enhanced cholinergic synaptic transmission in SHRs.
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Animais , Masculino , Ratos , Acetilcolina , Metabolismo , Pressão Sanguínea , Fisiologia , Sistema Cardiovascular , Metabolismo , Neurônios Colinérgicos , Metabolismo , Hipertensão , Metabolismo , Peptidil Dipeptidase A , Metabolismo , Ratos Endogâmicos SHR , MetabolismoRESUMO
Transcatheter renal sympathetic denervation with radiofrequency ablation has become a new treatment for refractory hypertension.Recent studies have showed that renal sympathetic denervation can also treat the diseases that are related to increased sympathetic nerve activity, such as metabolic diseases, cardiac disfunction, arrhythmia, obstructive sleep apnea syndrome, polycystic ovary syndrome, renal failure, etc. This paper aims to make a general review on the recent clinical research progress about renal sympathetic denervation with radiofrequency ablation.
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The arterial partial pressure (P CO2) of carbon dioxide is virtually constant because of the close match between the metabolic production of this gas and its excretion via breathing. Blood gas homeostasis does not rely solely on changes in lung ventilation, but also to a considerable extent on circulatory adjustments that regulate the transport of CO2 from its sites of production to the lungs. The neural mechanisms that coordinate circulatory and ventilatory changes to achieve blood gas homeostasis are the subject of this review. Emphasis will be placed on the control of sympathetic outflow by central chemoreceptors. High levels of CO2 exert an excitatory effect on sympathetic outflow that is mediated by specialized chemoreceptors such as the neurons located in the retrotrapezoid region. In addition, high CO2 causes an aversive awareness in conscious animals, activating wake-promoting pathways such as the noradrenergic neurons. These neuronal groups, which may also be directly activated by brain acidification, have projections that contribute to the CO2-induced rise in breathing and sympathetic outflow. However, since the level of activity of the retrotrapezoid nucleus is regulated by converging inputs from wake-promoting systems, behavior-specific inputs from higher centers and by chemical drive, the main focus of the present manuscript is to review the contribution of central chemoreceptors to the control of autonomic and respiratory mechanisms.
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Humanos , Neurônios Adrenérgicos/fisiologia , Fenômenos Fisiológicos Cardiovasculares , Células Quimiorreceptoras/fisiologia , Fenômenos Fisiológicos Respiratórios , Tronco Encefálico/fisiologia , Monóxido de Carbono/metabolismo , Sistema Nervoso Central/fisiologia , Bulbo/fisiologia , Ponte/fisiologia , Sistema Nervoso Simpático/fisiologiaRESUMO
Several forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.
Numerosas formas de evidência experimental obtidas nos últimos 37 anos demonstraram inequivocamente que a medula oblongata contém os principais circuitos responsáveis pela geração e manutenção do tono vasomotor e a regulação da pressão arterial. A visão atual que possuímos destes circuitos deriva em grande parte dos estudos de Pedro Guertzenstein, um estudante e mais tarde Professor de Fisiologia da UNIFESP e seus colaboradores. Nesta revisão nós sumarizamos os seus principais resultados assim como a nossa colaboração para uma melhor compreensão da regulação da pressão arterial em condições normais e patológicas.
Assuntos
Animais , Humanos , Ratos , Pressão Sanguínea/fisiologia , Hipertensão/fisiopatologia , Bulbo/fisiologia , Sistema Nervoso Simpático/fisiologia , Sistema Vasomotor/fisiologia , Barorreflexo/fisiologiaRESUMO
AIM:Left coronary artery ligation(LAD)was used to induce heart failure.Losartan was microinjected into paraventricular nucleus(PVN),heart rate(HR),blood pressure(BP)and renal sympathetic nerve activity(RSNA)were measured.The mechanism of PVN in chronic heart failure was investigated.METHODS:Sprague-Dawley male rats were selected for LAD ligation for heart failure models,the variation of cardiac function was detected by echocardiography.Losartan was microinjected into PVN,the responses of HR,BP and RSNA were analyzed.RESULTS:Compared with sham group,the level of LV was increased(P
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The purpose of this study was to assess an alteration of cardiac autonomic nerve activity during water immersion. Ten healthy young males (age : 21-28 yr.) were immersed in water at the temperatures of 25°C, 30°C and 34°C. Subjects sat calmly for 20 minutes in sitting position before water immersion, and then were immersed in water at subaxillary level in sitting position for 15 minutes, performing controlled breathing (15 cycle/min.) . Electrocardiograms were recorded continuously. Autonomic nerve activity was estimated with the analysis of power spectral by using the Fast Fourier Transformation (FFT) . High (HF ; 0.15-0.50 Hz) and low (LF ; 0.04-0.15 Hz) frequency areas and the ratio of LF to HF (LF/HF) were calculated as the indices of cardiac parasympathetic nerve activity, sympathetic nerve activity with parasympathetic modulation, and sympathetic nerve activity, respectively. During the water immersion at 25°C, 30°C and 34°C, HF was significantly increased, while the heart rate and LF/HF were significantly decreased. There were no statistically significant differences among both of HF and LF/HF during the immersion at 25°C, 30°C and 34°C, although the rate of change in HF at the temperature of 25°C appeared to be prominent compared to those at 30°C and 34°C and some subjects showed an exaggerated change in HF immediately after immersion. These results suggest that cardiac parasympathetic nerve activity is enhanced and cardiac sympathetic nerve activity is suppressed during a short time water immersion at the thermo-neutral temperature (34°C) and the temperatures of 25°C and 30°C, which are the usual temperatures found in indoor pools.
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A study was conducted to determine whether anticipation of exercise alters the responses of sympathetic nerve activity to muscle contraction. Sympathetic nerve activity leading to the skin (SSA) and muscle (MSA) was recorded from the tibial nerve in the left and right legs using tungsten microelectrodes. Heart rate and blood pressure (oscillometric method) were also measured during the experiment. Seven healthy subjects, who gave informed consent, participated in the experiment. They were asked to exert a static handgrip (SHG) for 2 min at a tension of 30% of maximal voluntary handgrip. Two different situations were set before the commencement of exercise. One was that after several minutes of controlled rest, a countdown was started 2 min before the exercise, and then the handgrip was applied (Cond. 1) . The other was that a preparation time of between 7 and 5 min was set prior to the handgrip exercise while no information regarding the starting time of exercise was given to the subjects (Cond. 2) . SSA for 30 s just before the exercise was increased in comparison with the control value at rest in Cond. 1, but not in Cond. 2. There was no difference in the SSA response patterns to SHG between the two conditions. Before the commencement of SHG, MSA did not alter from the control value at rest in either condition. The magnitudes of the increase in MSA during SHG were almost identical under both conditions. Heart rate for 30s before SHG in Cond. 1 was increased significantly from the control value, whereas there was no significant change in Cond. 2. The magnitude of the heart rate response to SHG was the same in both conditions. The mean blood pressure showed no significant change before SHG, but increased significantly during SHG in both conditions. The increases in SSA and heart rate prior to the commencement of exercise may be related to the anticipatory response to the exercise, although this response was not significant in MSA. These results confirm that anticipation of exercise increases sympathetic outflow to the skin. This may be advantageous in adapting the body to exercise.