Sympathetic System Activity Research Articles

Autonomic Modulation in Parkinson’s Disease Using Whole-Body Cryostimulation: A Pilot Study

Background: Parkinson’s disease (PD) is a multifaceted neurodegenerative disorder that progressively affects both the central and peripheral nervous systems. This pilot study aimed to examine the effects of repeated whole-body cryostimulation (WBC) sessions on the sympathovagal balance in PD patients and correlate heart rate variability (HRV) indexes with peripheral biomarkers of the autonomic nervous system (ANS). Methods: Seventeen PD patients with mild to moderate motor severity underwent a 10-session WBC cycle over 5 consecutive days. Thirteen patients (6 males, 7 females; mean age 64.5 ± 9.01 years; mean disease duration 5.4 ± 2.3 years) completed the protocol. Cardiac autonomic activity was assessed through HRV measures including RR interval variability (RR mean, RR min, RR max), power density of high and low frequencies (HF, LF), RMSSD, and the LF/HF ratio. Systemic sympathetic activity was evaluated via circulating blood catecholamine levels. Results: Significant increases were observed in RR mean, RR min, RR max, RMSSD, and HF spectrum, indicating enhanced parasympathetic activity. Blood pressure remained stable, suggesting safety. Conclusions: These findings provide initial support to WBC as a potential “rehabilitation booster” in PD, enhancing sympathovagal balance. Further research is needed to explore the long-term benefits of WBC in PD management.

Esaxerenone: blood pressure reduction and cardiorenal protection without reflex sympathetic activation in salt-loaded stroke-prone spontaneously hypertensive rats.

Mineralocorticoid receptor (MR) is involved in the mechanisms of blood pressure elevation, organ fibrosis, and inflammation. MR antagonists have been used in patients with hypertension, heart failure, or chronic kidney disease. Esaxerenone, a recently approved MR blocker with a nonsteroidal structure, has demonstrated a strong blood pressure-lowering effect. However, blood pressure reduction may lead to sympathetic activation through the baroreflex. The effect of esaxerenone on the sympathetic nervous system remains unclear. We investigated the effect of esaxerenone on organ damage and the sympathetic nervous system in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP), a well-established model of essential hypertension with sympathoexcitation and organ damage. Three-week administration of esaxerenone or hydralazine successfully attenuated the blood pressure elevation. Both esaxerenone and hydralazine comparably suppressed left ventricular hypertrophy and urinary albumin excretion. However, renal fibrosis and glomerular sclerosis were suppressed by esaxerenone but not hydralazine. Furthermore, plasma norepinephrine level, a parameter of systemic sympathetic activity, was significantly increased by hydralazine but not by esaxerenone. Consistent with these findings, the activity of the control centers of sympathetic nervous system, the parvocellular region of the paraventricular nucleus in the hypothalamus and the rostral ventrolateral medulla, was enhanced by hydralazine but remained unaffected by esaxerenone. These results suggest that esaxerenone effectively lowers blood pressure without inducing reflex sympathetic nervous system activation. Moreover, the organ-protective effects of esaxerenone appear to be partially independent of its blood pressure-lowering effect. In conclusion, esaxerenone demonstrates a blood pressure-lowering effect without concurrent sympathetic activation and exerts organ-protective effects in salt-loaded SHRSP. Esaxerenone has antihypertensive and cardiorenal protective effects without reflex sympathetic activation in salt-loaded stroke-prone spontaneously hypertensive rats.

Short-term meditation training alters brain activity and sympathetic responses at rest, but not during meditation

Although more people are engaging in meditation practices that require specialized training, few studies address the issues associated with nervous activity pattern changes brought about by such training. For beginners, it remains unclear how much practice is needed before objective physiological changes can be detected, whether or not they are similar across the novices and what are the optimal strategies to track these changes. To clarify these questions we recruited individuals with no prior meditation experience. The experimental group underwent an eight-week Taoist meditation course administered by a professional, while the control group listened to audiobooks. Both groups participated in audio-guided, 34-min long meditation sessions before and after the 8-week long intervention. Their EEG, photoplethysmogram, respiration, and skin conductance were recorded during the mediation and resting state periods. Compared to the control group, the experimental group exhibited band-specific topically organized changes of the resting state brain activity and heart rate variability associated with sympathetic system activation. Importantly, no significant changes were found during the meditation process prior and post the 8-week training in either of the groups. The absence of notable changes in CNS and ANS activity indicators during meditation sessions, for both the experimental and control groups, casts doubt on the effectiveness of wearable biofeedback devices in meditation practice. This finding redirects focus to the importance of monitoring resting state activity to evaluate progress in beginner meditators. Also, 16 h of training is not enough for forming individual objectively different strategies manifested during the meditation sessions. Our results contributed to the development of tools to objectively monitor the progress in novice meditators and the choice of the relevant monitoring strategies. According to our findings, in order to track early changes brought about by the meditation practice it is preferable to monitor brain activity outside the actual meditation sessions.

Beneficial effects of renal denervation on heart, kidneys, and adipose tissue beyond antihypertensive effect: is it independent of systemic sympathetic activity?

Beneficial effects of renal denervation on heart, kidneys, and adipose tissue beyond antihypertensive effect: is it independent of systemic sympathetic activity?

β-Adrenergic Receptor Blockade Augments Sympathetically Mediated Vasoconstriction during Hypoxia in Healthy Young Adults

Objective: Vascular tone is dictated by the net balance of vasodilatory and vasoconstrictor influences. During hypoxia, systemic sympathetic vasoconstrictor activity is increased but peripheral vasodilation prevails — suggesting vasodilatory factors outweigh sympathetically-mediated vasoconstrictor influences in the healthy state. Given vascular β-adrenergic receptors contribute to hypoxic vasodilation, we hypothesized pharmacological blockade of β-adrenergic receptors would augment the vasoconstrictor response to acute sympathetic activation during hypoxia. Methods: Thirteen young healthy participants (5F/8M, 27±7 yr, 25±3 kg/m2) completed two study visits randomized and blinded to oral placebo or propranolol (1mg/kg, NCT05256069). On each visit, participants completed two trials: 1) 10-min normoxia (0.21 FiO2, 98±0% SpO2) followed by sympathetic activation via a 2-min normoxic cold pressor test (CPT); 2) 5-min steady-state hypoxia (0.10±0.01 FiO2, 81±1% SpO2) followed by a 2-min hypoxic CPT. Forearm blood flow (FBF, venous occlusion plethysmography) and blood pressure (BP, finger photoplethysmography) were assessed. FBF was normalized for mean BP (forearm vascular conductance, FVC). A change in FVC from steady-state to the last 1-min of CPT was calculated (ΔFVC = CPT − steady-state) and expressed as a percent change (%FVC = ΔFVC/steady-state x 100). Results: The vascular response to sympathetic activation (CPT) was unaffected by hypoxia under placebo conditions (normoxia: -34±21%; hypoxia: -29±32%, p=0.33). In contrast, following β-adrenergic blockade with oral propranolol, sympathetically-mediated vasoconstriction was augmented during hypoxia (normoxia: -29±30%; hypoxia: -40±27%, p=0.04). Conclusion: β-adrenergic receptor blockade augments the vasoconstrictor response to acute sympathetic activation during hypoxia in a mixed-sex cohort. These preliminary data indicate functional β-adrenergic receptors are required to restrain sympathetically-mediated vasoconstriction during hypoxia. Based on data supporting sex-related differences in adrenergic control of vascular tone, future work will seek to stratify results by sex. Funding: AHA 909014 (DWJ), APS-SURF (BJB), HL153523 (JKL). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Afferent Renal Denervation Attenuates Sympathetic Overactivation From the Paraventricular Nucleus in Spontaneously Hypertensive Rats.

The effectiveness of renal denervation (RDN) in reducing blood pressure and systemic sympathetic activity in hypertensive patients has been established. However, the underlying central mechanism remains unknown. This study aimed to investigate the role of RDN in regulating cardiovascular function via the central renin-angiotensin system (RAS) pathway. Ten-week-old spontaneously hypertensive rats (SHR) were subjected to selective afferent renal denervation (ADN) using capsaicin solution. We hypothesized that ADN would effectively reduce blood pressure and rebalance the RAS component of the paraventricular nucleus (PVN) in SHR. The experimental results show that the ADN group exhibited significantly lower blood pressure, reduced systemic sympathetic activity, decreased chronic neuronal activation marker C-FOS expression in the PVN, and improved arterial baroreflex function, compared with the Sham group. Furthermore, ACE and AT1 protein expression was reduced while ACE2 and MAS protein expression was increased in the PVN of SHR after ADN. These findings suggest that RDN may exert these beneficial effects through modulating the central RAS pathway.

Vaccines in cardiology, an underutilized strategy to reduce the residual cardiovascular risk.

Cardiovascular diseases stand as the leading cause of mortality among adults globally. For decades, comprehensive evidence has underscored the correlation between infections, particularly those involving the respiratory system, and an elevated risk of cardiovascular and cerebrovascular events, as well as all-cause mortality. The mechanisms through which infections heighten cardiovascular events are intricate, encompassing immune system activation, systemic inflammation, hypercoagulable states, sympathetic system activation, and increased myocardial oxygen demand. Respiratory infections further contribute hypoxemia to this complex interplay. These mechanisms intertwine, giving rise to endothelial dysfunction, plaque ruptures, myocardial depression, and heart failure. They can either instigate de novo cardiovascular events or exacerbate pre-existing conditions. Compelling evidence supports the safety of influenza, pneumococcal, herpes zoster, COVID-19 and respiratory syncytial virus vaccines in individuals with cardiovascular risk factors or established cardiovascular disease. Notably, the influenza vaccine has demonstrated safety even when administered during the acute phase of a myocardial infarction in individuals undergoing angioplasty. Beyond safety, these vaccinations significantly reduce the incidence of cardiovascular events in individuals with an augmented cardiovascular risk. Nevertheless, vaccination rates remain markedly suboptimal. This manuscript delves into the intricate relationship between infections and cardiovascular events. Additionally, we highlight the role of vaccinations as a tool to mitigate these occurrences and reduce residual cardiovascular risk. Finally, we emphasize the imperative need to optimize vaccination rates among individuals with heart diseases.

High platelet adrenergic activity and concomitant activation of the pituitary/medullar axis as alarming laboratory parameters in ACS survivors-the STRESS-AMI study.

Kinetics of stress-related biological parameters were determined in acute coronary syndrome (ACS) patients undergoing complex cardiovascular rehabilitation. We determined platelet functionality in the absence/presence of a selective alpha-2 adrenergic receptor inhibitor, atipemazole parallel with salivary cortisol levels at enrolment, and at 3- and 12-months follow-up in 75 ACS patients with percutaneous coronary intervention. Pharmacological/non-pharmacological secondary prevention methods have been efficiently applied. Baseline aggregometry indicated platelet hyperactivity, decreasing gradually and being significantly reduced late, at 12 months (p < 0.05). Cortisol levels followed similar kinetics (p < 0.05). Baseline epinephrine-induced aggregations (EIA) significantly correlated with most of the other platelet agonists, even at subsequent time-points. Patients with upper-quartile EIA at enrolment (EIA-UQ) had significantly higher ADP- and collagen-induced aggregations at enrolment, at 3- and 12-months follow-up as well, indicating that high adrenergic response in the acute phase is accompanied by general platelet hyperactivity and predicts sustained platelet activation. In the EIA-UQ group higher cardiac biomarker release, elevated C-reactive protein and cortisol levels, and lower baseline left ventricular ejection fraction were detected.Atipemazole significantly reduced platelet aggregation induced by several platelet agonists, being most potent and comparable to full in vitro P2Y12 inhibition on collagen-induced aggregations (p < 0.05), indicating that catecholamines might serve as promt/long-term modulators of platelet function. Despite effective CCR programme and dual antiplatelet therapy, prolonged activation of sympathetic neuroendocrine system and general platelet hyperactivity can be detected up to one year in ACS patients with high adrenergic platelet activity. Moreover, initial high adrenergic activity is accompanied by clinical parameters associated to increased cardiovascular risk, therefore early identification of these patients might support complex optimal long-term therapy.

Pupillometry to show stress release during equine sports massage therapy

Anecdotal reports state that wellness treatments for horses, such as massage therapy, relaxes the treated animal. Massage therapists and horse owners typically report an ”improvement” without verifying or quantifying the treatment results. This paper shows that the effect of wellness treatment and stress release can be measured with pupillometry. One of the horse’s pupils was photographed at the beginning and end of the treatment to determine the changes in the balance between the sympathetic and parasympathetic system activities. The owners assigned horses to two experimental groups: animals receiving a massage (N = 18) and horses standing with a person next to the horse for the time of a massage in the stable lane (N = 10). Six animals in the experimental group were excluded from the analysis because the pupils could not be traced. We opened the images of the pupil with Fiji (ImageJ) and used the elliptical selection tool to measure the pupils’ and iris’ areas. The ratio between the pupils’ aperture and the iris’ area was a normalized measure for pupil size. At the end of the experiment, we compared the normalized size of the pupils with a two-tailed paired t-test within groups and a two-tailed t-test between groups. For the experimental group, it was before and after the treatment, and for the control group, before and after the horse was placed in the stable lane. Comparisons between the experimental and control groups were made at the procedure's beginning and end. The treatment significantly decreased the normalized pupil area in the experimental group, on average, by a factor of 0.78 ± 0.15 (P = 0.042). For the horses in the control group, the pupil size increased, on average, by a factor of 1.14 ± 018. Changes were statistically not significant (P = 0.19). The initial pupil size of the horses in the experimental group was 1.88 times larger than that in the control group. After the treatment, the difference was reduced to a factor of 1.25. At the beginning of the experiment, the horses in the experimental group had, on average, larger pupil sizes than the horses in the control group, indicating that the horses in the experimental group were more stressed before the treatment than the control animals. The observed changes in pupil size in the experimental group likely resulted from enhanced parasympathetic and diminished sympathetic activity resulting from the treatment. Observed changes in pupil size agree with the anecdotal horse owner reports and the therapist’s treatment notes.

Study Protocol for the Pleiotropic Effects of Sodium-Glucose Cotransporter2 Inhibitor on Organ-Specific Sympathetic Nerve Activity and Insulin Sensitivity in Participants with Type2 Diabetes.

Hyperinsulinemia and hyperglycemia are associated with exaggerated systemic sympathetic nerve activity (SNA) in patients with type2 diabetes. Sodium-glucose cotransporter2 (SGLT2) inhibitors lower insulin levels, whereas sulfonylureas increase insulin levels. We will test whether these two classes of antidiabetic agents have different effects on SNA. The present study is an ongoing, 24-week, one-center (only Kanazawa University Hospital), open-label, randomized, parallel trial (jRCTs 041200035). Participants with type2 diabetes with multiple atherosclerosis risk factors are randomly assigned in a 1:1 manner to receive 2.5mg luseogliflozin or 0.5mg glimepiride once daily. The sample size was calculated to be 14 in each group, with a significance level of 0.05 and a power of 0.80. The design required 40 evaluable study participants. Our primary endpoint will be the change in muscle SNA (MSNA). The secondary endpoints included organ-specific insulin sensitivity measured by a hyperinsulinemic-euglycemic clamp study using an artificial pancreas combined with a stable isotope-labeled glucose infusion, bioelectrical impedance analysis, and organ-specific (cardiac, renal, and hepatic) 123I-meta-iodobenzylguanidine (MIBG) innervation imaging. Study recruitment started in April 2020 and will end in June 2024, with 40 participants randomized into the two groups. The treatment follow-up of the participants is currently ongoing and is due to finish by March 2025. The study protocol has been approved by the Certified Review Board, Kanazawa University, Ishikawa, Japan, in accordance with the guidelines stipulated in the Declaration of Helsinki (CRB4180005, 2019-001). This trial is registered with the Japan Registry of Clinical Trials, jRCTs 041200035.

The relationship between periodic limb movement during sleep and dyslipidaemia in patients with obstructive sleep apnea.

Periodic limb movements during sleep and obstructive sleep apnea are both associated with increased sympathetic tone, and have been proposed as risk factors for heart diseases and, in particular, cardiovascular disease. As sympathetic system activation may lead to dyslipidaemia, periodic limb movements during sleep could be an additional risk factor for cardiovascular disease in patients with obstructive sleep apnea. The aim of the study was to determine whether the presence of periodic limb movements during sleep affects serum lipid levels in obstructive sleep apnea. Total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, non- high-density lipoprotein cholesterol and triglyceride levels were investigated in 4138 patients with obstructive sleep apnea in the European Sleep Apnea Database (ESADA) cohort, divided into those with periodic limb movements during sleep index ≥ 15 per hr (n = 628) and controls (n = 3510). ANCOVA adjusted for age, sex, body mass index, apnea-hypopnea index, alcohol intake, smoking status, diabetes, insomnia and study site was used to assess differences in lipids between periodic limb movements during sleep and controls. Patients with periodic limb movements during sleep (24% female, 54.4 ± 12.1 years, body mass index 31.9 ± 5.8 kg m-2 , apnea-hypopnea index 36.7 ± 25.4 per hr) had higher triglyceride (1.81 ± 1.04 versus 1.69 ± 0.90 mmol L-1 , p = 0.002) and lower high-density lipoprotein cholesterol (1.19 ± 0.34 versus 1.24 ± 0.37 mmol L-1 , p = 0.002) levels, whilst there was no difference in either total cholesterol (4.98 ± 1.10 versus 4.94 ± 1.07 mmol L-1 ), low-density lipoprotein cholesterol (3.04 ± 0.96 versus 2.98 ± 0.98 mmol L-1 ) or non- high-density lipoprotein cholesterol (3.78 ± 1.10 versus 3.70 ± 1.05 mmol L-1 ) concentrations (all p > 0.05). The results remained unchanged after most sensitivity analyses. Patients with obstructive sleep apnea with periodic limb movements during sleep had more prevalent cardiovascular disease (11% versus 6%, p < 0.01). Periodic limb movements during sleep in obstructive sleep apnea is associated with dyslipidaemia independently of important confounders. Our results highlight periodic limb movements during sleep as an additional risk factor for cardiovascular disease in obstructive sleep apnea.

Mitochondrial Damage and Hypertension: Another Dark Side of Sodium Excess.

Essential or primary hypertension (HT) is a worldwide health problem with no definitive cure. Although the exact pathogenesis of HT is not known, genetic factors, increased renin-angiotensin and sympathetic system activity, endothelial dysfunction, oxidative stress, and inflammation play a role in its development. Environmental factors such as sodium intake are also important for BP regulation, and excess sodium intake in the form of salt (NaCl, sodium chloride) increases blood pressure in salt-sensitive people. Excess salt intake increases extracellular volume, oxidative stress, inflammation, and endothelial dysfunction. Recent evidence suggests that increased salt intake also disturbs mitochondrial function both structurally and functionally which is important as mitochondrial dysfunction is associated with HT. In the current review, we have summarized the experimental and clinical data regarding the impact of salt intake on mitochondrial structure and function. Excess salt intake damage mitochondrial structure (e.g., shorter mitochondria with less cristae, increased mitochondrial fission, increased mitochondrial vacuolization). Functionally, high salt intake impairs mitochondrial oxidative phosphorylation and electron transport chain, ATP production, mitochondrial calcium homeostasis, mitochondrial membrane potential, and mitochondrial uncoupling protein function. Excess salt intake also increases mitochondrial oxidative stress and modifies Krebs cycle protein expressions. Studies have shown that high salt intake impairs mitochondrial structure and function. These maladaptive mitochondrial changes facilitate the development of HT especially in salt-sensitive individuals. High salt intake impairs many functional and structural components of mitochondria. These mitochondrial alterations along with increased salt intake promote the development of hypertension.

Sympathetic nervous activation, mitochondrial dysfunction and outcome in acutely decompensated cirrhosis: the metabolomic prognostic models (CLIF-C MET)

Background and aimsCurrent prognostic scores of patients with acutely decompensated cirrhosis (AD), particularly those with acute-on-chronic liver failure (ACLF), underestimate the risk of mortality. This is probably because systemic inflammation...

Stressfulness of the design influences consistency of cognitive measures and their correlation with animal personality traits in wild mice (Mus musculus)

Individual variation in cognition is being increasingly recognized as an important evolutionary force but contradictory results so far hamper a general understanding of consistency and association with other behaviors. Partly, this might be caused by external factors imposed by the design. Stress, for example, is known to influence cognition, with mild stress improving learning abilities, while strong or chronic stress impairs them. Also, there might be intraspecific variation in how stressful a given situation is perceived. We investigated two personality traits (stress coping and voluntary exploration), spatial learning with two mazes, and problem-solving in low- and high-stress tests with a group of 30 female wild mice (Mus musculus domesticus). For each test, perceived stress was assessed by measuring body temperature change with infrared thermography, a new non-invasive method that measures skin temperature as a proxy of changes in the sympathetic system activity. While spatial learning and problem-solving were found to be repeatable traits in mice in earlier studies, none of the learning measures were significantly repeatable between the two stress conditions in our study, indicating that the stress level impacts learning. We found correlations between learning and personality traits; however, they differed between the two stress conditions and between the cognitive tasks, suggesting that different mechanisms underlie these processes. These findings could explain some of the contradictory findings in the literature and argue for very careful design of cognitive test setups to draw evolutionary implications.

Hyponatraemia caused by transient syndrome of inappropriate antidiuresis to urinary retention.

Hyponatraemia is frequently seen in the emergency department, possibly caused by thesyndromeofinappropriate antidiuresis (SIAD). We report three cases in which we believe urinary retention with bladder distention caused hyponatraemia. Laboratory findings fulfilled the criteria for SIAD, for which no cause was found. Possibly pain or sympathetic nerve system activation leads to SIAD. Brisk diuresis occurred after placement of an indwelling urinary catheter with overly correction of sodium for which treatment was necessary. Clinicians should be aware that placement of an indwelling urinary catheter may prompt brisk water diuresis and a tendency to overcorrection.

Effect of Low T3 Syndrome on Severity of Coronary Artery Disease in Patients with Acute Coronary Syndrome: A Cross-sectional Study

Introduction: Low Triiodothyronine (T3) syndrome is a hormonal imbalance that significantly influences cardiovascular haemodynamics by altering the vascular endothelial function by influencing the Nitric Oxide (NO) production. In Acute Coronary Syndrome (ACS) inflammation disrupts plaque which stimulates thrombosis, coagulation, activation of sympathetic system and release of cytokines mainly Interleukin 6 (IL-6), which is a pleotropic and pro-inflammatory cytokine, which exerts inhibitory effect on thyroid axis function. Aim: To study the association of low T3 syndrome and severity of Coronary Artery Disease (CAD) in ACS. Materials and Methods: This cross-sectional study was conducted in the Intensive Critical Care Unit (ICCU)under the Department of Cardiology, Karnataka institute of Medical Sciences, Hubli, Karnataka, India, from July 2021 to August 2022. A total of 120 consecutive ACS patients were taken for the study and all underwent Coronary Angiography (CAG). Severity of CAD was assessed with the help of Gensini risk scoring system. The patients were divided based on thyroid function status. Low T3 syndrome was defined as &lt;0.846 ng/ mL with normal values of Thyroxine (T4) and Thyroid Stimulating Hormone (TSH). Receiver operating characteristic curves were generated to correlate low T3 syndrome and angiographic severity of CAD. Multinominal logistic regression analysis demonstrated LT3S is an independent risk factor for CAD. The Chi-square test was used for ordered categorical data with the severity of coronary artery lesions. Results: The severity of coronary artery lesions in the low T3 syndrome group (n=29, 24.16%) and hypothyroidism (n=20, 16.6%) group was significantly greater than that of euthyroid group (n=71, 59.1%), with all the groups’ (p-value=0.047). Multinominal logistic regression analysis demonstrated that low T3 syndrome was an independent risk factor of CAD for moderate (Odds ratio=2.34, 95%CI: 0.47-11.39, p&lt;0.02) and severe (Odds ratio=8.56, 95%CI: 1.52-47.9, p&lt;0.015) lesions. Conclusion: The patients with low T3 syndrome are associated with more severe and diffuse CAD and low T3 syndrome is an independent risk factor for ACS.

The impact of yogic practices on perception of stress and sleep among medical students amid COVID-19 pandemic

Background: Medical undergraduates struggled to cope up with undue stress resulting in disturbed sleep during COVID-19 pandemic. Stress had affected not only the mental or psychological health but also affected the whole body systems including the sleep rhythm and quality. This study was undertaken focusing on the fact that yogic practices induce changes in stress level and sleep. Aims and Objectives: The aim of the study was to measure and compare the perceived stress and sleep quality among the medical undergraduate who discontinued and those who continued yogic practices in follow-up. Materials and Methods: This online longitudinal interventional study was conducted from November 2020 to May 2021. The study was conducted in three stages: Baseline (before intervention). after 6 weeks of yogic intervention, and after 3 months (for follow-up). All medical students of 18–30 years were enrolled (Total 600 students). Fifty-one undergraduate with prolonged illness, spine issues, any physiological issue, trained athletes, and trained yoga persons were excluded from the study. Total 549 medical students were falling in our inclusion criteria. Results: Significant level of stress response is a high predictor of poor sleep because of HPA mediated hormonal and sympathetic system activation. High level of stress is a significant predictor of poor quality of sleep. This causes persistent production of cortisol and epinephrine. Intervention of yogic practice helps in balancing the mind and body, thus improving the quality of life. Conclusion: The authors findings suggest that the undergraduates are in favor of practicing yoga as it helps them to cope up with the academic stress. It had also improved the quality of sleep among them.

The Dosage Effect of Laser Acupuncture at PC6 (Neiguan) on Heart Rate Variability: A Pilot Study.

Laser acupuncture (LA) has been more applicated in the clinical practice with good responses, but the dosage and parameter settings are still inconsistent with the arguments. This study is focused on the effect of LA on heart rate variability (HRV) with different energy density (ED). Based on the Arndt-Schulz law, we hypothesized that the effective range should fall within 0.01 to 10 J/cm2 of ED, and settings above 10 J/cm2 would perform opposite or inhibitory results. We recruited healthy adults in both sexes as subjects and choose bilateral PC6 (Neiguan) as the intervention points to observe the HRV indexes changes by an external wrist autonomic nerve system (ANS) watch on the left forearm. The data from the ANS watch, including heart rate, blood pressure, and ANS activity indexes, such as low frequency (LF), high frequency (HF), LF%, HF%, LF/HF ratio, and so on, were analyzed by the one-way ANOVA method to test the possible effect. In this study, every subject received all three different EDs of LA in a randomized order. After analyzing the data of 20 subjects, the index of HF% was upward and LF/HF ratio was downward when the ED was 7.96 J/cm2. Otherwise, the strongest ED 23.87 J/cm2 performed the opposite reaction. Appropriately, LA intervention could affect the ANS activities, with the tendency to increase the ratio of parasympathetic and decrease the ratio of sympathetic nerve system activities with statistically significant results, and different ED interventions are consistent with Arndt-Schulz law with opposite performance below and above 10 J/cm2.

Contribution of afferent renal nerve signals to acute and chronic blood pressure regulation in stroke-prone spontaneously hypertensive rats.

The activation of sympathetic nervous system plays a critical role in the development of hypertension. The input from afferent renal nerves may affect central sympathetic outflow; however, its contribution to the development of hypertension remains unclear. We investigated the role of afferent renal nerves in acute and chronic blood pressure regulation using normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Acute chemical stimulation of afferent renal nerves elicited larger increases in blood pressure and renal sympathetic nerve activity in young 9-week-old SHRSP compared to WKY. Selective afferent renal denervation (ARDN) and conventional total renal denervation (TRDN) ablating both afferent and efferent nerves in young SHRSP revealed that only TRDN, but not ARDN, chronically attenuated blood pressure elevation. ARDN did not affect plasma renin activity or plasma angiotensin II levels, whereas TRDN decreased both. Neither TRDN nor ARDN affected central sympathetic outflow and systemic sympathetic activity determined by neuronal activity in the parvocellular region of hypothalamic paraventricular nucleus and rostral ventrolateral medulla and by plasma and urinary norepinephrine levels, respectively. Renal injury was not apparent in young SHRSP compared with WKY, suggesting that renal afferent input might not be activated in young SHRSP. In conclusion, the chronic input from afferent renal nerves does not contribute to the development of hypertension in SHRSP despite the increased blood pressure response to the acute stimulation of afferent renal nerves. Efferent renal nerves may be involved in the development of hypertension via activation of the renin-angiotensin system in SHRSP.

The novel anti-colitic effect of β-adrenergic receptors via modulation of PS1/BACE-1/Aβ axis and NOTCH signaling in an ulcerative colitis model.

Although dysautonomia was documented in inflammatory bowel disease, with activation of the stress-related sympathetic system, the role of agonists/antagonists of the adrenergic receptors is not conclusive. Moreover, ulcerative colitis was recently linked to dementia, but the potential role of the presenilin 1(PS1)/BACE-1/beta-amyloid (Aβ) axis has not been evaluated. Hence, we investigated the impact of mirabegron (β3-agonist) and/or carvedilol (β1/β2 antagonist) on iodoacetamide-induced ulcerative colitis with emphasis on the novel pathomechanism of the PS1/BACE-1/Aβ axis in ulcerative colitis, and its relation to the inflammatory cascade, fibrotic processes, and the gut barrier dysfunction. Ulcerated rats were either left untreated or treated for 8days with mirabegron and/or carvedilol. Besides minimizing colon edema and weight loss, and improving colon structure, mirabegron and/or carvedilol abated colonic PS1/BACE-1/Aβ axis and the NOTCH1/NICD/HES1 hub besides the inflammatory cascade GSK3-β/NF-κΒ/TNF-α, and the oxidative stress marker malondialdehyde. The anti-fibrotic effect was verified by boosting SMAD-7 and inhibiting TGF-β1, α-SMA immunoexpression, and MTC staining. Moreover, the drugs improved the gut barrier function, attested by the increased goblet cells and expression of E-cadherin, and the inhibited expression of p (Y654)-β-catenin to preserve the E-cadherin/β-catenin adherens junction (AJ). These signaling pathways may be orchestrated by the replenished PPAR-γ, a transcription factor known for its anti-colitic effect. Conclusion: Besides maintaining the gut barrier, mirabegron and/or carvedilol mediated their anti-colitic effect by their anti-oxidant, anti-inflammatory, and anti-fibrotic capacities. The therapeutic effect of these drugs depends partly on suppressing the harmful signaling pathways PS1/BACE-1/Aβ, NOTCH1/NICD/HES1, GSK3-β/NF-κΒ/TNF-α, and TGF-1β/α-SMA while enhancing PPAR-γ, SMAD-7, mucus, and AJ.