Modulation Of Autonomic Activity Research Articles

Beneficial Effects of Vestibular Exercise Along with Yoga on Diabetes Mellitus: A Review

Diabetes Mellitus (DM) is becoming one of the major growing health issues due to an unhealthy lifestyle. DM can be controlled through regular yoga practice. Yoga has a therapeutic effect on DM and other metabolic disorders. Vestibular exercises (VE) are a type of exercise concerned with the stimulation of the vestibular system. Studies show Vestibular stimulation will prevent DM and associated complications. Vestibular exercises are also a part of yoga but it is not using in yoga therapy for DM. The inclusion of Vestibular exercises in diabetic yoga may effective for DM patients. Regular yoga practice can prevent or delay the development of DM by increasing glucose uptake by cells, reducing oxidative stress, improving physical fitness, reducing stress, etc... Vestibular stimulation also reduces the chance of DM by increasing insulin secretion through vagal stimulation and sympathetic inhibition, reducing stress, modulation of autonomic activity, promoting sleep, etc. A combination of Vestibular exercise and Yoga postures may give a combined effect of both. So it is beneficial rather than Vestibular exercise alone or yoga postures alone.

Nitric oxide in the insular cortex modulates baroreflex responses in a cGMP-independent pathway

Insular cortex is a brain structure involved in the modulation of autonomic activity and cardiovascular function. The nitric oxide/cyclic guanosine-3′,5′-monophosphate pathway is a prominent signaling mechanism in the central nervous system, controlling behavioral and physiological responses. Nevertheless, despite evidence regarding the presence of nitric oxide-synthesizing neurons in the insular cortex, its role in the control of autonomic and cardiovascular function has never been reported. Thus, the present study aimed to investigate the involvement of nitric oxide/cyclic guanosine-3′,5′-monophosphate pathway mediated by neuronal nitric oxide synthase (nNOS) activation within the insular cortex in the modulation of baroreflex responses in unanesthetized rats. For this, we evaluated the effect of bilateral microinjection of either the nitric oxide scavenger carboxy-PTIO, the selective neuronal nitric oxide synthase inhibitor Nω-Propyl-l-arginine or the soluble guanylate cyclase inhibitor ODQ into the insular cortex on the bradycardia evoked by blood pressure increases in response to intravenous infusion of phenylephrine, and the tachycardia caused by blood pressure decreases evoked by intravenous infusion of sodium nitroprusside. Bilateral microinjection of either NPLA or carboxy-PTIO into the insular cortex increased the reflex bradycardic response, whereas the reflex tachycardia was decreased by these treatments. Bilateral microinjection of the soluble guanylate cyclase inhibitor into the insular cortex did not affect any parameter of baroreflex function evaluated. Overall, our findings provide evidence that insular cortex nitrergic signaling, acting via neuronal nitric oxide synthase, plays a prominent role in control of baroreflex function. However, control of reflex responses seems to be independent of soluble guanylate cyclase activation.

Diet-Induced Metabolic Syndrome Reduced Heart Rate Variability and Increased Irregularity and Complexity of Short-Term RR Time Series in Rabbits.

Simple SummaryIn recent years, obesity and metabolic syndrome (MetS) have become more prevalent, owing to increased unhealthy habits and sedentary lifestyles becoming public health problems. Both conditions are linked with a higher prevalence of sudden cardiac death (SCD), but the exact mechanisms are not known. An autonomic nervous system imbalance can produce atrial and ventricular arrhythmias, which cause SCD, and this can be quantified by analyzing heart rate variability (HRV). We investigated HRV using time-domain, frequency-domain and nonlinear analyses during the development of MetS in rabbits and found HRV modifications that could be associated with the higher prevalence of SCD in this pathological condition.Metabolic syndrome (MetS) has been linked to a higher prevalence of sudden cardiac death (SCD), but the mechanisms are not well understood. One possible underlying mechanism may be an abnormal modulation of autonomic activity, which can be quantified by analyzing heart rate variability (HRV). Our aim was to investigate the modifications of short-term HRV in an experimental rabbit model during the time-course of MetS development. NZW rabbits were randomly assigned to a control (n = 10) or a MetS group (n = 13), fed 28 weeks with control or high-fat, high-sucrose diets. After anesthesia, a 15-min ECG recording was acquired before diet administration and at weeks 14 and 28. We analyzed short RR time series using time-domain, frequency-domain and nonlinear analyses. A mixed-model factorial ANOVA was used for statistical analysis. Time-domain analysis showed a 52.4% decrease in the standard deviation of heart rate in animals from the MetS group at week 28, but no changes in the rest of parameters. In the frequency domain, we found a 9.7% decrease in the very low frequency and a 380.0% increase of the low frequency bands in MetS animals at week 28, whereas high frequency remained unchanged. Nonlinear analyses showed increased complexity and irregularity of the RR time series in MetS animals.

Cerebral Aβ40 and systemic hypertension

Mid-life hypertension and cerebral hypoperfusion may be preclinical abnormalities in people who later develop Alzheimer’s disease. Although accumulation of amyloid-beta (Aβ) is characteristic of Alzheimer’s disease and is associated with upregulation of the vasoconstrictor peptide endothelin-1 within the brain, it is unclear how this affects systemic arterial pressure. We have investigated whether infusion of Aβ40 into ventricular cerebrospinal fluid modulates blood pressure in the Dahl salt-sensitive rat. The Dahl salt-sensitive rat develops hypertension if given a high-salt diet. Intracerebroventricular infusion of Aβ induced a progressive rise in blood pressure in rats with pre-existing hypertension produced by a high-salt diet (p < 0.0001), but no change in blood pressure in normotensive rats. The elevation in arterial pressure in high-salt rats was associated with an increase in low frequency spectral density in systolic blood pressure, suggesting autonomic imbalance, and reduced cardiac baroreflex gain. Our results demonstrate the potential for intracerebral Aβ to exacerbate hypertension, through modulation of autonomic activity. Present findings raise the possibility that mid-life hypertension in people who subsequently develop Alzheimer’s disease may in some cases be a physiological response to reduced cerebral perfusion complicating the accumulation of Aβ within the brain.

Early Impairment of central modulation of autonomic activity in neurodegenerative disorders

Early Impairment of central modulation of autonomic activity in neurodegenerative disorders

Modulation of autonomic activity in neurological conditions: Epilepsy and Tourette Syndrome.

This manuscript considers the central but neglected role of the autonomic nervous system in the expression and control of seizures in epilepsy (small) and tics in Tourette Syndrome (TS). In epilepsy, consideration of autonomic involvement is typically confined to differential diagnoses (e.g., syncope), or in relation to Sudden Unexpected Death in Epilepsy (SUDEP). Investigation is more limited in Tourette Syndrome. The role of the autonomic nervous system in the generation and prevention of epileptic seizures is largely overlooked. Emotional stimuli such as anxiety and stress are potent causes of seizures and tic activity in epilepsy and TS, respectively. This manuscript will describe a possible neural mechanism by which afferent autonomic projections linked to cognition and behavior influence central thalamo-cortical regulation, which appears to be an important means for controlling both seizure and tic activity. It also summarizes the link between the integrity of the default mode network and autonomic regulation in patients with epilepsy as well as the link between impaired motor control and autonomic regulation in patients with TS. Two neurological conditions; epilepsy and TS were chosen, as seizures and tics represent parameters that can be easily measured to investigate influences of autonomic functions. The EDA biofeedback approach is anticipated to gain a strong position within the next generation of treatment for epilepsy, as a non-invasive technique with minimal side effects. This approach also takes advantage of the current practical opportunity to utilize growing digital health technology.

Neuroticism Modifies Psychophysiological Responses to Fearful Films

BackgroundNeuroticism is a personality component frequently found in anxious and depressive psychiatric disorders. The influence of neuroticism on negative emotions could be due to its action on stimuli related to fear and sadness, but this remains debated. Our goal was thus to better understand the impact of neuroticism through verbal and physiological assessment in response to stimuli inducing fear and sadness as compared to another negative emotion (disgust).MethodsFifteen low neurotic and 18 high neurotic subjects were assessed on an emotional attending task by using film excerpts inducing fear, disgust, and sadness. We recorded skin conductance response (SCR) and corrugator muscle activity (frowning) as indices of emotional expression.ResultsSCR was larger in high neurotic subjects than in low neurotics for fear relative to sadness and disgust. Moreover, corrugator activity and SCR were larger in high than in low neurotic subjects when fear was induced.ConclusionAfter decades of evidence that individuals higher in neuroticism experience more intense emotional reactions to even minor stressors, our results indicate that they show greater SCR and expressive reactivity specifically to stimuli evoking fear rather than to those inducing sadness or disgust. Fear processing seems mainly under the influence of neuroticism. This modulation of autonomic activity by neurotics in response to threat/fear may explain their increased vulnerability to anxious psychopathologies such as PTSD (post traumatic stress disorder).

RELATIVE ROLE OF OBESITY AND OCCUPATIONAL HAZARDS ON AUTONOMIC MODULATION

In the present day world every occupation induces various degrees of stress on individual although the perception may vary in individual to individual and in certain occupation it is greatest and such occupations are called hazardous occupation. The driver who is taking driving as a profession and exposed in transport industry also has to do shift work. Stress induces a wide range of physiological and or behavioral changes that have evolved along phylogeny which take place under different situations 1 . Shift work is associated with an increased rate of cardiovascular disease and accidents. Discordance between circadian rhythm of stress related biological variables and the work sleep schedule explains the reduced efficiency of work. In obese persons we see increased sympathetic modulation of arterial pressure. Studies showed that there was a decreased LF and HF component of HRV in obese individual when compared with normal 11 . Spectral analysis showed that obese individual will have low LF component. This low LF power of heart rate reflects the diminished adrenocepter responsiveness 12 . Thus both obesity and driving (hazardous occupation) have got profound adverse effect on autonomic activity. The present study was devised to evaluate the chief determinant factor among these drivers in the modulation of autonomic activity.

The Prorenin and (Pro)renin Receptor: New Players in the Brain Renin-Angiotensin System?

It is well known that the brain renin-angiotensin (RAS) system plays an essential role in the development of hypertension, mainly through the modulation of autonomic activities and vasopressin release. However, how the brain synthesizes angiotensin (Ang) II has been a debate for decades, largely due to the low renin activity. This paper first describes the expression of the vasoconstrictive arm of RAS components in the brain as well as their physiological and pathophysiological significance. It then focus on the (pro)renin receptor (PRR), a newly discovered component of the RAS which has a high level in the brain. We review the role of prorenin and PRR in peripheral organs and emphasize the involvement of brain PRR in the pathogenesis of hypertension. Some future perspectives in PRR research are heighted with respect to novel therapeutic target for the treatment of hypertension and other cardiovascular diseases.

An update on pain physiology: the relevance of Craig's and Jänig's hypotheses for hypnotic analgesia

AbstractThe aim of the present review is to discuss two interesting hypotheses that explain the pathophysiology of pain: (1) Arthur Craig's hypothesis that the experience of pain, elicited by specific sensors projecting into the central nervous system through afferent pathways, is relevant for homeostasis and represents a specific emotion related to a homeostatic behavioural drive; and (2) Wilfrid Jänig's hypothesis that, in functional chronic pain syndromes, specific changes occur in autonomic, endocrine and somatic motor systems interactions which, then, result in dysregulation involving peripheral, spinal and brain mechanisms. Theoretically, on the basis of these two hypotheses, hypnotic suggestions for analgesia can affect pain at multiple levels, including its generation at the periphery, secondary sensory neurons sensitization, and modulation of endocrine/immune responses through the modulation of autonomic activity. Copyright © 2009 British Society of Experimental &amp; Clinical Hypnosis. Published by John Wiley &amp; Sons, Ltd.

Autonomic and electrophysiological correlates of emotional intensity in older and younger adults

Anterior cingulate cortex (ACC) is involved in the modulation of autonomic activity, emotional responsivity, and the monitoring of goal-directed behavior. However, these functions are rarely studied together to determine how they relate or whether their pattern of relation changes with age. We recorded respiratory sinus arrhythmia (RSA), an index of autonomic activity, error-related event related potentials (ERN/Pe), generated in ACC, and the self-reported intensity of 5 basic emotions in older and younger adults. Emotional intensity did not differ with age. The ERN/Pe and RSA were reduced with age and related specifically to sadness intensity for both groups. When examined together, RSA accounted for the relation between ERN/Pe and sadness. This is consistent with a model of medial prefrontal function in which autonomic processes mediate the relation between cognitive control and affective regulation, a pattern that also did not differ with age.

Respiratory modulation of the autonomic nervous system during Cheyne–Stokes respirationThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum.

Cheyne-Stokes respiration (CSR) is associated with increased mortality among patients with heart failure. However, the specific link between CSR and mortality remains unclear. One possibility is that CSR results in excitation of the sympathetic nervous system. This review relates evidence that CSR exerts acute effects on the autonomic nervous system during sleep, and thereby influences a number of cardiovascular phenomena, including heart rate, blood pressure, atrioventricular conduction, and ventricular ectopy. In patients in sinus rhythm, heart rate and blood pressure oscillate during CSR in association with respiratory oscillations, such that both peak heart rate and blood pressure occur during the hyperpneic phase. Inhalation of CO2 abolishes both CSR and the associated oscillations in heart rate and blood pressure. In contrast, O2 inhalation sufficient to eliminate hypoxic dips has no significant effect on CSR, heart rate, or blood pressure. In patients with atrial fibrillation, ventricular rate oscillates in association with CSR despite the absence of within-breath respiratory arrhythmia. The comparison of RR intervals between the apneic and hyperpneic phases of CSR indicates that this breathing disorder exerts its effect on ventricular rate by inducing cyclical changes in atrioventricular node conduction properties. In patients with frequent ventricular premature beats (VPBs), VPBs occur more frequently during the hyperpneic phase than the apneic phase of CSR. VPB frequency is also higher during periods of CSR than during periods of regular breathing, with or without correction of hypoxia. In summary, CSR exerts multiple effects on the cardiovascular system that are likely manifestations of respiratory modulation of autonomic activity. It is speculated that the rhythmic oscillations in autonomic tone brought about by CSR may ultimately contribute to the sympatho-excitation and increased mortality long observed in patients with heart failure and CSR.

P-440 Modulation of autonomic activity and mortality in patients with congestive heart failure

P-440 Modulation of autonomic activity and mortality in patients with congestive heart failure

P-440 Modulation of autonomic activity and mortality in patients with congestive heart failure

P-440 Modulation of autonomic activity and mortality in patients with congestive heart failure

Modulation of Autonomic Activity Preceding Postoperative Atrial Fibrillation

Modulation of Autonomic Activity Preceding Postoperative Atrial Fibrillation

Differential modulation of autonomic activity by ethmozin and ethacizin (analog of ethmozin) on the canine sinus node and atrioventricular junction

The chronotropic and dromotropic actions of ethmozin and its diethylamine analog ethacizin were studied in the presence and absence of combined muscarinic, beta- and alpha-adrenoreceptor blockade in the intact canine heart in situ (n = 38). Injections of ethacizin, 5, 10 and 25 micrograms/ml, into the sinus node artery caused an immediate and significant (p less than 0.001) sinus bradycardia of 2, 6 and 11%, respectively. Injection of 25 and 50 micrograms/ml of ethacizin into the atrioventricular (AV) node artery significantly (p less than 0.001) prolonged AV conduction time with occasional second degree heart block. Conduction delay was located exclusively during the AH interval of the His bundle electrogram. Autonomic blockade did not alter the negative chronotropic or negative dromotropic effects of ethacizin. Ethacizin, 25 micrograms/ml, injected into the sinus node artery immediately reduced the sinus node response to vagal stimulations by 30% and the effect of acetylcholine, 0.1 micrograms/ml, injected into the sinus node artery by 50%. Ethacizin, 25 micrograms/ml, injected into the AV node artery immediately reduced the duration of complete AV block elicited by vagal stimulation or intranodal acetylcholine, 0.5 micrograms/ml, by 90%. Ethacizin caused a minor reduction in sinus node response to right stellate stimulations without, however, altering the sinus node response to intranodal norepinephrine. Ethmozin injections of up to 50 micrograms/ml into the sinus and AV node arteries had no chronotropic or dromotropic effects. Ethmozin had a minor and variable vagolytic action but significantly (p less than 0.05) reduced the sinus node response to sympathetic nerve stimulation. Hence, ethacizin, in contrast to ethmozin, has a direct depressing action on both the sinus node and the AV junction.(ABSTRACT TRUNCATED AT 250 WORDS)