Sympathetic Nervous System Activity Research Articles

Severity of depressive symptoms moderates the sympathoinhibitory effect of local skin warming following exposure to a social stressor

Depression is the leading cause of disease burden globally. Existing antidepressant treatments that target the central nervous system have limited efficacy and come at the cost of significant side effects. Thus, there is growing interest in novel therapeutic interventions for the prevention and treatment of depression, including interventions that target interoceptive signaling. The thermosensory system may hold particular promise, given evidence that depression is associated with impairments in thermosensory functioning, and that whole-body hyperthermia produces an antidepressant effect in patients with major depressive disorder. In this study, we investigated whether the severity of depressive symptoms in a non-clinical population moderated the effect of local skin warming on subjective and physiological stress responses following exposure to an acute social stressor. Following exposure to the stressor, participants (N = 90) rested their arm on a heat blanket that was either turned on (local skin warming condition) or left off (control condition). We demonstrate that local skin warming increased fingertip temperature, a marker of reduced sympathetic nervous system activity, but only for participants with high levels of depressive symptoms. While local skin warming also inhibited salivary alpha amylase, severity of depressive symptoms did not moderate this effect, and no effect was found for electrodermal activity. These data highlight the importance of incorporating peripheral physiology in our conceptualization of the pathophysiology of depression and show that changes in sympathetic nervous system activity may underpin the antidepressant effect of warm stimuli.

It's cool to be stressed: Body surface temperatures track sympathetic nervous system activation during acute stress.

The acute stress response can be considered the primary evolutionary adaptation to maximise fitness in the face of unpredictable environmental challenges. However, the difficulties of assessing physiology in natural environments mean comparatively little is known about how response variation influences fitness in free-living animals. Currently, determining acute stress physiology typically involves blood sampling or cardiac monitoring. Both require trapping and handling, interrupting natural behaviour, and potentially biasing our understanding toward trappable species/individuals. Importantly, limits on repeated sampling also restrict response phenotype characterisation, vital for linking stress with fitness. Surface temperature dynamics resulting from peripheral vasomotor activity during acute stress are increasingly promoted as alternative physiological stress indicators, which can be measured non-invasively using infrared thermal imaging, overcoming many limitations of current methods. Nonetheless, which aspects of stress physiology they represent remains unclear, as the underlying mechanisms are unknown. To date, validations have primarily targeted the hypothalamic-pituitary-adrenal axis, when the sympathetic-adrenal-medullary (SAM) system is likely the primary driver of vasomotor activity during acute stress. To address this deficit, we compared eye and bill region surface temperatures - measured using thermal imaging - with SAM system activity - measured as heart-rate-variability via electrocardiogram telemetry - in wild-caught captive house sparrows (Passer domesticus), during capture and handling. We found lower body surface temperatures were associated with increased sympathetic nervous system activation. Consequently, our data confirm body surface temperatures can act as a proxy for sympathetic activation during acute stress, providing potentially transformative opportunities for linking the acute stress response with fitness in the wild.

The Sympathetic Nervous System in Hypertensive Heart Failure with Preserved LVEF.

The neurohormonal model of heart failure (HF) pathogenesis states that a reduction in cardiac output caused by cardiac injury results in sympathetic nervous system (SNS) activation, that is adaptive in the short-term and maladaptive in the long-term. This model has proved extremely valid and has been applied in HF with a reduced left ventricular (LV) ejection fraction (LVEF). In contrast, it has been undermined in HF with preserved LVEF (HFpEF), which is due to hypertension (HTN) in the vast majority of the cases. Erroneously, HTN, which is the leading cause of cardiovascular disease and premature death worldwide and is present in more than 90% of HF patients, is tightly linked with SNS overactivity. In this paper we provide a contemporary overview of the contribution of SNS overactivity to the development and progression of hypertensive HF (HHF) as well as the clinical implications resulting from therapeutic interventions modifying SNS activity. Throughout the manuscript the terms HHF with preserved LVEF and HfpEF will be used interchangeably, considering that the findings in most HFpEF studies are driven by HTN.

Acute repeated cage exchange stress modifies urinary stress and plasma metabolic profiles in male mice.

Exposure to a novel environment is psychologically and physically stressful for humans and animals. The response has been reported to involve enhanced sympathetic nervous system activity, but changes in nutrient levels under stress are not fully understood. As a form of exposure to a novel environment, repeated cage exchange (CE, four times at 2-h intervals for 8 h from 08:00 h) during the light phase with no restraint on movement was applied to A/J mice, a strain particularly prone to stress. Body temperature was measured with a temperature-sensing microchip implanted in the interscapular region. The stress conditions and anxiety level were evaluated by measuring urinary catecholamines and corticosterone and by performing an anxiety-like behavior test, respectively. Major nutrients such as glucose, fatty acids, and amino acids in the plasma were also examined. CE mice showed a significant increase in body temperature with each CE. They also showed a significantly greater reduction of body weight change, more water intake, and higher levels of urinary catecholamines and corticosterone and anxiety-like behavior score than control mice. The model revealed a significantly lower plasma glucose level and higher levels of several essential amino acids, such as branched-chain amino acids and phenylalanine, than those of control mice. Meanwhile, free fatty acids and several amino acids such as arginine, aspartic acid, proline, threonine, and tryptophan in both sets of mice were significantly decreased from the corresponding levels at 08:00 h, while similar plasma levels were exhibited between mice with and without CE. In conclusion, repeated CE stress was associated with changes in glucose and amino acids in plasma. Although further study is needed to clarify how these changes are specifically linked to anxiety-like behavior, this study suggests the potential for nutritional intervention to counter stress in humans exposed to novel environments.

Triglyceride, an Independent Risk Factor for New-Onset Hypertension: A Perspective.

Hypertension is the most important risk factor for cardiovascular disease worldwide. Although the pathogenesis of hypertension is complex and multifactorial, obesity-related hypertension has become a major focus of attention because of the continued increase in the prevalence of overweight and obesity. Several mechanisms have been suggested to underlie obesity-related hypertension, including an increase in sympathetic nervous system activity, an upregulation of the renin-angiotensinaldosterone system, alterations in adipose-derived cytokines, and an augmentation of insulin resistance. Emerging evidence from observational studies (including those using Mendelian randomization) suggests that the presence of high triglycerides, which is a common comorbidity in obesity, is an independent risk factor for new-onset hypertension. However, little is known about the mechanisms underlying triglyceride-associated hypertension. We summarize the existing clinical evidence that has demonstrated the adverse effect of triglycerides on blood pressure, and we then discuss possible underlying mechanisms based on the evidence from animal and human studies, with a particular focus on the roles of endothelial function, white blood cells, i.e., lymphocytes, and pulse rate.

Role of ventrolateral part of ventromedial hypothalamus in post-myocardial infarction cardiac dysfunction induced by sympathetic nervous system

Psychological stress has been recognized as a contributing factor to worsened prognosis in patients with cardiac failure following myocardial infarction (MI). Although the ventrolateral part of the ventromedial hypothalamus (VMHVL) has been implicated in emotional distress, its involvement in post-MI cardiac dysfunction remains largely unexplored. This study was designed to investigate the effect of the VMHVL activation in the MI rat model and its underlying mechanisms. Our findings demonstrate that activation of VMHVL neurons enhances the activity of the cardiac sympathetic nervous system through the paraventricular nucleus (PVN) and superior cervical ganglion (SCG). This activation leads to an elevation in catecholamine levels, which subsequently modulates myosin function and triggers the release of anti-inflammatory factors, to exacerbate the post-MI cardiac prognosis. The denervation of the superior cervical ganglion (SGN) effectively blocked the cardiac sympathetic effects induced by the VMHVL activation, and ameliorated the cardia fibrosis and dysfunction. Therefore, our study identified the role of the “VMHVL-PVN-SCG” sympathetic pathway in the post-MI heart, and proposed SGN as a promising strategy in mitigating cardiac prognosis in stressful rats.

A preliminary investigation of salivary α-amylase as a novel biomarker of subjective response to alcohol: A brief report.

Alcohol misuse represents a universal public health concern that spans multiple demographics. As such, understanding shared, biological indicators of alcohol-related risk is vital to implementing targeted prevention and intervention efforts. Self-report measures of subjective response to alcohol (SR) capture both psychological and pharmacological effects of alcohol and robustly predict patterns of alcohol use, negative consequences, and the development of alcohol use disorders. Importantly, several biological markers of alcohol's sedating effects, including cortisol, have been identified and complement subjective response assessments. However, biological markers of alcohol's stimulating effects are less understood. Studies have implicated alcohol-induced changes in heart rate as a viable marker, but heart rate measurements are susceptible to measurement error. Salivary α-amylase, a reliable indicator of sympathetic nervous system activation, represents a promising alternative biomarker of alcohol-induced stimulation. Using data from a large, placebo-controlled alcohol administration study (N = 448), the present study examined the extent to which α-amylase is a viable marker of alcohol-induced stimulation. To test this, a measurement model was estimated in which baseline and ascending limb subjective stimulation latent variables were created using two validated measures of subjective response. Ascending self-reports of stimulation and levels of α-amylase were then regressed onto beverage conditions and allowed to correlate with each other. Findings indicated that α-amylase is sensitive to acute alcohol consumption and is positively, but not statistically reliably, related to the ascending limb stimulant SR. Future studies should consider including salivary α-amylase as a noninvasive physiological indicator of alcohol's stimulating effects. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Chronic stress induces pulmonary epithelial cells to produce acetylcholine that remodels lung pre-metastatic niche of breast cancer by enhancing NETosis

BackgroundChronic stress promotes most hallmarks of cancer through impacting the malignant tissues, their microenvironment, immunity, lymphatic flow, etc. Existing studies mainly focused on the roles of stress-induced activation of systemic sympathetic nervous system and other stress-induced hormones, the organ specificity of chronic stress in shaping the pre-metastatic niche remains largely unknown. This study investigated the role of chronic stress in remodeling lung pre-metastatic niche of breast cancer.MethodsBreast cancer mouse models with chronic stress were constructed by restraint or unpredictable stress. Expressions of tyrosine hydroxylase, vesicular acetylcholine transporter (VAChT), EpCAM and NETosis were examined by immunofluorescence and confocal microscopy. mRNA and protein levels of choline acetyltransferase (ChAT), VAChT, and peptidylarginine deiminase 4 were detected by qRT-PCR and Western blotting, respectively. Immune cell subsets were analyzed by flow cytometry. Acetylcholine (ACh) and chemokines were detected by ELISA and multi chemokine array, respectively. ChAT in lung tissues from patients was examined by immunohistochemistry.ResultsBreast cancer-bearing mice suffered chronic stress metastasized earlier and showed more severe lung metastasis than did mice in control group. VAChT, ChAT and ChAT+ epithelial cells were increased significantly in lung of model mice undergone chronic stress. ACh and chemokines especially CXCL2 in lung culture supernatants from model mice with chronic stress were profoundly increased. Chronic stress remodeled lung immune cell subsets with striking increase of neutrophils, enhanced NETosis in lung and promoted NETotic neutrophils to capture cancer cells. ACh treatment resulted in enhanced NETosis of neutrophils. The expression of ChAT in lung tissues from breast cancer patients with lung metastasis was significantly higher than that in patients with non-tumor pulmonary diseases.ConclusionsChronic stress promotes production of CXCL2 that recruits neutrophils into lung, and induces pulmonary epithelial cells to produce ACh that enhances NETosis of neutrophils. Our findings demonstrate for the first time that chronic stress induced epithelial cell derived ACh plays a key role in remodeling lung pre-metastatic niche of breast cancer.

The Five Basic Human Senses Evoke Electrodermal Activity.

Electrodermal activity (EDA) usually relates to variations in the electrical properties of palmar or plantar skin sites. EDA responses, namely skin conductance responses (SCRs), skin potential responses (SPRs) and skin susceptance responses (SSRs) are shown to be sensitive indexes of sympathetic nervous system activation and are studied in many research projects. However, the association between EDA responses and the five basic human senses has not been investigated yet. Our study aimed to explore the relationship between the three EDA responses (SCRs, SSRs and SPRs) and the five basic human senses. These three EDA responses were measured simultaneously at the same skin site on each of the 38 volunteers. The tested five senses were sight, hearing, touch, taste and smell. The results showed that the different tested senses led to different degrees of EDA responses due to activation of the sympathetic nervous system and corresponding secretion of sweat. Although a controlled study on the degree of EDA as a function of the strength of each stimulus was not performed, we noted that the largest EDA responses were typically associated with the smell sense test. We conclude that EDA responses could be utilized as measures for examining the sensitivity of the human senses. Hence, EDA devices may have important roles in sensory systems for future clinical applications.

PEP reward reactivity moderates the effects of RSA reactivity on antisocial behavior and substance use.

Integrating Polyvagal Theory and Reinforcement Sensitivity Theory (RST), we examined pre-ejection period (PEP) reward reactivity, which was suggested to index trait impulsivity, as a moderator between respiratory sinus arrhythmia (RSA) reactivity and antisocial behavior (ASB), and substance use in an urban male, adult sample. To understand the inconsistent findings between RSA reactivity and externalizing problems, we proposed to study both negatively and positively valenced tasks for RSA reactivity and to include PEP reward reactivity as a moderator for the RSA-behavior link. Data were collected from an urban sample of 131 male adults (active offenders, demographic controls, and college students). ICG (impedance cardiography) and ECG (electrocardiogram) were recorded, computing PEP (sympathetic nervous system activity marker) and RSA (parasympathetic nervous system activity marker), while participants completed the modified Trier Social Stress Test and a simple reward task. Reactivity was calculated by subtracting the baseline from the task activity. Consistent with prior studies, more RSA withdrawal to stress and less PEP shortening to reward predicted the most ASB and substance use. Less RSA withdrawal to reward and more PEP shortening to reward predicted the most ASB and substance use. We incorporated autonomic space, RST, and Polyvagal Theory to discuss our findings, and specifically highlight how clarifying what each reactivity captures based on the task demand (e.g., presence of social threat, need for vagal-mediated social affiliative behavior) can illuminate our understanding of the result patterns.

Effects of inhaled low-concentration xenon gas on naltrexone-precipitated withdrawal symptoms in morphine-dependent mice

BackgroundOpioid withdrawal symptoms (OWS) are highly aversive and prompt unprescribed opioid use, which increases morbidity, mortality, and, among individuals being treated for opioid use disorder (OUD), recurrence. OWS are driven by sympathetic nervous system (SNS) hyperactivity that occurs when blood opioid levels wane. We tested whether brief inhalation of xenon gas, which inhibits SNS activity and is used clinically for anesthesia and diagnostic imaging, attenuates naltrexone-precipitated withdrawal-like signs in morphine-dependent mice. MethodsAdult CD-1 mice were implanted with morphine sulfate-loaded (60 mg/ml) minipumps and maintained for 6 days to establish morphine dependence. On day 7, mice were given subcutaneous naltrexone (0.3 mg/kg) and placed in a sealed exposure chamber containing either 21% oxygen/balance nitrogen (controls) or 21% oxygen/added xenon peaking at 30%/balance nitrogen. After 10 minutes, mice were transferred to observation chambers and videorecorded for 45 minutes. Videos were scored in a blind manner for morphine withdrawal behaviors. Data were analyzed using 2-way ANOVAs testing for treatment and sex effects. Results and conclusionsXenon-exposed mice exhibited fewer jumps (P = 0.010) and jumping suppression was detectible within the first 10-minute video segment, but no sex differences were detected. Brief inhalation of low concentration xenon rapidly and substantially attenuated naltrexone-precipitated jumping in morphine-dependent mice, suggesting that it can inhibit OWS. If xenon effects translate to humans with OUD, xenon inhalation may be effective for reducing OWS, unprescribed opioid use, and for easing OUD treatment initiation, which could help lower excess morbidity and mortality associated with OUD.

Pilot study shows skin-to-skin care with parents improves heart rate variability in preterm infants in the neonatal intensive care unit.

Skin-to-skin care in the newborn intensive care unit typically lasts for short periods of time and enhances breastfeeding, attachment, and parental self-esteem. Heart rate variability (HRV) increases with gestational age and is a measure of maturation of parasympathetic vs. sympathetic autonomic nervous system activity. HRV measurements may be useful in capturing changes in autonomic regulation in response to skin-to-skin care. To analyze the effects of skin-to-skin care on HRV in preterm infants receiving respiratory support. We hypothesized that skin-to-skin care would result in a more mature pattern of parasympathetic activity. In this prospective crossover study, infants <30 weeks' gestation and 1-6 weeks postnatal age had HRV recorded for 30 min before, during, and after skin-to-skin care sessions. HRV characteristics analyzed included the standard deviation of the normal-to-normal interval (SDNN), the root mean squared of successive differences of normal-to-normal intervals (RMSSD), and the standard deviation of decelerations (SDDec). 10 infants between 25 5/7-29 6/7 weeks gestational age and 7-41 days postnatal age completed 22 sessions while receiving respiratory support (positive pressure ventilation or nasal cannula oxygen). Two measures of HRV (SDNN and RMSSD) were significantly decreased by the end of the skin-to-skin sessions, compared to pre-session values. SDNN decreased from a median of 10.44 ms before the session to 6.70 ms after being placed back in bed (p < 0.05), with RMSSD decreasing from a median of 6.80 ms before the session to 4.32 ms while being held at the end of 30 min (p < 0.05). Skin-to-skin care with a parent resulted in a more mature autonomic nervous system pattern in preterm infants receiving respiratory support, suggesting physiologic benefit for the infant. No adverse events were seen during any session.

Sympathetic nervous system responses to acute psychosocial stress in male physicians with clinical burnout

BackgroundOccupational burnout has been associated with an increased risk of cardiovascular disease, with sympathetic nervous system (SNS) dysfunction as one explanation. This study examined the effects of burnout on responses of SNS activity measures to acute psychosocial stress in male physicians, a population at risk for burnout. MethodsStudy participants were 60 male physicians, 30 with clinical burnout, assessed with the Maslach Burnout Inventory, and 30 without burnout (controls). All participants underwent the 15-min Trier Social Stress Test. Heart rate, blood pressure, salivary alpha-amylase, and plasma levels of epinephrine (EPI) and norepinephrine were assessed pre-stress, immediately post-stress, and 15 min and 45 min post-stress. ResultsPhysicians with burnout and controls differed in EPI changes over time, controlling for age, job stress and anxiety symptoms (F (3,147) = 5.18, p = .002 for 'Time by Group' interaction; η2p = .096). Burnout was associated with a smaller increase in EPI from pre-stress to immediately post-stress (r(54) = −.40, p = .004). The emotional exhaustion dimension of burnout was a significant driver of this effect. The area under the curve with respect to increase in EPI was also smaller in the burnout group (F (1,49) = 6.06, p = .017, η2p = .110). Group differences were not significant for the other SNS activity measures. ConclusionsBurnout may be linked to dysfunction of the sympathoadrenal medullary (SAM) system, when exposed to acute psychosocial stress. In keeping with the allostatic load concept, an insufficient SAM stress response in burnout could potentially contribute to cardiovascular disease.

The sympathetic nervous system in heart failure revisited.

Several attempts have been made, by the scientific community, to develop a unifying hypothesis that explains the clinical syndrome of heart failure (HF). The currently widely accepted neurohormonal model has substituted the cardiorenal and the cardiocirculatory models, which focused on salt-water retention and low cardiac output/peripheral vasoconstriction, respectively. According to the neurohormonal model, HF with eccentric left ventricular (LV) hypertrophy (LVH) (systolic HF or HF with reduced LV ejection fraction [LVEF] or HFrEF) develops and progresses because endogenous neurohormonal systems, predominantly the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS), exhibit prolonged activation following the initial heart injury exerting deleterious hemodynamic and direct nonhemodynamic cardiovascular effects. However, there is evidence to suggest that SNS overactivity often preexists HF development due to its association with HF risk factors, is also present in HF with preserved LVEF (diastolic HF or HFpEF), and that it is linked to immune/inflammatory factors. Furthermore, SNS activity in HF may be augmented by coexisting noncardiac morbidities and modified by genetic factors and demographics. The purpose of this paper is to provide a contemporary overview of the complex associations between SNS overactivity and the development and progression of HF, summarize the underlying mechanisms, and discuss the clinical implications as they relate to therapeutic interventions mitigating SNS overactivity.

Propranolol treatment during repetitive mild traumatic brain injuries induces transcriptomic changes in the bone marrow of mice.

There are 1.5 million new mild traumatic brain injuries (mTBI) annually in the US, with many of the injured experiencing long-term consequences lasting months after the injury. Although the post injury mechanisms are not well understood, current knowledge indicates peripheral immune system activation as a causal link between mTBI and long-term side effects. Through a variety of mechanisms, peripheral innate immune cells are recruited to the CNS after TBI to repair and heal the injured tissue; however, the recruitment and activation of these cells leads to further inflammation. Emerging evidence suggests sympathetic nervous system (SNS) activity plays a substantial role in the recruitment of immune cells post injury. We sought to identify the peripheral innate immune response after repeated TBIs in addition to repurposing the nonselective beta blocker propranolol as a novel mTBI therapy to limit SNS activity and mTBI pathophysiology in the mouse. Mice underwent repetitive mTBI or sham injury followed by i.p. saline or propranolol. Isolated mRNA derived from femur bone marrow of mice was assayed for changes in gene expression at one day, one week, and four weeks using Nanostring nCounter® stem cell characterization panel. Differential gene expression analysis for bone marrow uncovered significant changes in many genes following drug alone, mTBI alone and drug combined with mTBI. Our data displays changes in mRNA at various timepoints, most pronounced in the mTBI propranolol group, suggesting a single dose propranolol injection as a viable future mTBI therapy in the acute setting.

The Anti-Inflammatory Action of Pulsed Radiofrequency-A Hypothesis and Potential Applications.

In 2013, it was reported that pulsed radiofrequency (PRF) could be applied to obtain a systemic anti-inflammatory effect. Patients with chronic pain and patients with an inflammatory condition from other disciplines could potentially profit from this finding. At that time, intravenous application was used, but since then, it became clear that it could be applied transcutaneously as well. This procedure was named RedoxPRF. This can be used both for regional and for systemic application. Recently, the basic element of the mode of action has been clarified from the analysis of the effects of PRF on a standard model of muscle injury in rats. The objective of this paper is to present a hypothesis on the mode of action of RedoxPRF now that the basic mechanism has become known. Cell stress causes an increased production of free radicals, disturbing the redox equilibrium, causing oxidative stress (OS) either directly or secondarily by other types of stress. Eventually, OS causes inflammation and an increased sympathetic (nervous) system activity. In the acute form, this leads to immune paralysis; in the chronic form, to immune tolerance and chronic inflammation. It is hypothesized that RedoxPRF causes a reduction of free radicals by a recombination of radical pairs. For systemic application, the target cells are the intravascular immune cells that pass through an activated area as on an assembly line. Hypothesis conclusions: 1. RedoxPRF treatment works selectively on OS. It has the unique position of having a point of engagement at the most upstream level of the train of events. 2. RedoxPRF has the potential of being a useful tool in the treatment of inflammatory diseases and possibly of stage 4 cancer. 3. In the treatment of chronic pain, RedoxPRF is an entirely new method because it is different from ablation as well as from stimulation. We propose the term "functional restoration". 4. Controlled studies must be conducted to develop this promising new field in medicine further.

Randomized Trial Comparing SGLT2 Inhibition and Hydrochlorothiazide on Sympathetic Traffic in Type 2 Diabetes

Reductions in sympathetic nervous system activity may contribute to beneficial effects of sodium glucose cotransporter 2 (SGLT2) inhibition on cardiovascular outcomes. Therefore, we tested the hypothesis that SGLT2 inhibition with empagliflozin (Empa) lowers muscle sympathetic nerve activity (MSNA) in patients with type 2 diabetes mellitus (T2DM) compared with hydrochlorothiazide (HCT) to discern SGLT2-specific actions from responses to increased natriuresis. We randomized patients with T2DM on metformin monotherapy to either 25 mg/d Empa (n= 20) or 25 mg/d HCT (n= 21) for 6 weeks in a parallel, double-blind fashion. We assessed MSNA by peroneal microneurography, blood pressure, cardiovascular and metabolic biomarkers at baseline and at the end of treatment. Both drugs elicited volume depletion, as indicated by increased thoracic impedance. Compared with HCT, Empa caused 1.23 kg more body weight loss (P= 0.011) and improved glycemic control. Seated systolic blood pressure decreased with both treatments (P< 0.002). MSNA did not change significantly with either treatment; however, MSNA changes were negatively correlated with changes in body weight on Empa (P= 0.042) and on HCT(P= 0.001). The relationship was shifted to lower MSNA on Empa compared with HCT (P= 0.002). Increased renal sodium excretion eliciting body weight loss may promote sympathetic activation. However, sympathetic excitation in the face of increased sodium loss may be attenuated by SGLT2 inhibitor-specific actions.

Endovascular ultrasound renal denervation to lower blood pressure in young hypertensive women planning pregnancy: study protocol for a multicentre randomised, blinded and sham controlled proof of concept study

IntroductionA major issue confronting clinicians treating hypertension in pregnancy is the limited number of pharmacological options. Endovascular catheter-based renal denervation (RDN) is a new method to lower blood pressure (BP)...

Prediction of Arousal and Valence State from Electrodermal Activity using Wavelet based ResNet50 Model

Abstract Real time physiological signals like Electrodermal Activity (EDA), measured using wearable devices, could be used for emotion recognition, thus enabling new paradigms of health monitoring, including mental health. This paper analyses EDA signals, a measure of sympathetic nervous system activity, which plays a significant role in emotional regulation. A public database was used to categorize emotions based on valence and arousal values. The Continuous Wavelet Transform (CWT) was used to obtain the scalograms of the signals. The scalograms were then fed into the deep learning models, VGG16 and ResNet50, to recognize emotions. VGG16 gives a Pearson Linear Correlation Coefficient (PLCC) value of 0.7199 for valence and 0.7593 for arousal, with Mean Absolute Error (MAE) and Root Mean Square Error (RMSE) values of 0.7653 and 1.0284, respectively. ResNet50 performs better, with a PLCC value of 0.7763 for valence and 0.8207 for arousal, and lower MAE and RMSE values of 0.7158 and 0.8712, respectively. This study proposes an adapted ResNet50 model for emotion recognition which could be integrated into wearable devices as a prospective feature.

Effects of Respiratory Muscle Exercise on Blood Pressure Response by Sympathetic Nervous System Activation

PURPOSE: This study investigated the cardiovascular improvement effect of respiratory muscle exercise and evaluate the possibility of improving and preventing cardiovascular disease (CVD) from a long-term perspective.METHODS: The study was designed as a crossover design with the same subjects (n=9). Subjects underwent a 2-week non-intervention period (CON) and a 2-week respiratory muscle exercise period (RespEX). Body composition, blood pressure, heart rate (HR), and inspiratory capacity were measured for all subjects before and after the intervention. In addition, cold pressure test (CPT) and exercise stress test were performed.RESULTS: Respiratory muscle exercise was found to significantly reduce resting HR (in RespEX, Pre- vs. Post-, &lt;i&gt;p&lt;/i&gt;&lt;.01). This was accompanied by the strengthening of the respiratory muscles. Also, exercise time was increased (in RespEX, Pre- vs. Post-, &lt;i&gt;p&lt;/i&gt;&lt;.001). However, it did not induce an increase in maximal oxygen consumption. The results of the CPT confirmed that hypersensitivity-induced HR increases were prevented.CONCLUSIONS: Respiratory muscle exercise may have some benefits in preventing CVD, but it seems reasonable to use it as an adjunctive therapy to aerobic exercise. Although limited, it was confirmed that respiratory muscle exercise can have a beneficial effect on cardiovascular improvement and CVD prevention through CPT.