Sympathetic Attenuation Research Articles

Exercise training ameliorates adrenergic control in spontaneously hypertensive rats

ABSTRACT The goal of this study was to examine vascular control after sympathetic stimulation by tyramine infusion in hypertensive rats submitted to swimming training. To this end, male rats were assigned to the following groups: sedentary (SN) and trained normotensive (TN), sedentary (SH) and trained hypertensive (TH). Arterial pressure (AP), heart rate (HR), HR variability (HRV), AP variability (APV), and cardiac autonomic function were recorded. Following, infusion of tyramine was administrated. The TN and TH showed a lower resting HR compared with their respective sedentary groups (p < .05). Pressure levels were less in TH than SH (p < .05). The TH showed a higher HRV together with a lower APV in comparison to SH (p < .05). The sympathetic modulation of HRV and APV was lower in TH than in SH (p < .05). Both trained groups presented an increased parasympathetic modulation of HRV compared with their respective sedentary groups (p < .05). The TN and TH groups had a higher vagal effect in comparison with their respective sedentary groups (p < .001). The sympathetic effect was lower in TH than in SH (p < .001). Pressor and HR responses to tyramine in different doses were attenuated in TH (p < .001). Further analysis showed a significant association between infusion of tyramine and normalized LF component of HRV (r = 0.84, p < .001), systolic APV (r = 0.58, p < .001) and diastolic APV (r = 0.49, p < .001). In conclusion, exercise training provokes less pressor response variation by tyramine infusion in hypertensive animals suggesting sympathetic nerve endings adjustments and decrease of the vasoconstrictor effect attenuates injury caused by hypertension improving cardiovascular autonomic dysfunction, which can be associated with sympathetic attenuation.

High frequency heart rate variability evoked by repetitive transcranial magnetic stimulation over the medial prefrontal cortex: A preliminary investigation on brain processing of acute stressor-evoked cardiovascular reactivity

Introduction: Transcranial Magnetic Stimulation (TMS) is a non-invasive technique for brain stimulation. Repetitive TMS (rTMS) over the medial Prefrontal Cortex (mPFC), Broadman Area 10 (BA10) may stimulate transynaptically perigenual Anterior Cingulate Cortex (pACC, BA 33), insula, amigdala, hypothalamus and connected branches of the Autonomic Nervous System (ANS) involved in stressorevoked cardiovascular reactivity. Stressors are associated with an increase in sympathetic cardiac control, a decrease in parasympathetic control, or both, and, consequently, an increase in systolic/stroke volume, total vascular impedance/resistance and heart rate, a decrease of baroreflex sensitivity, i.e., an increase in blood pressure/arterial tension. Objectives and Aims: The present work aims, using TMS and accordingly to Gianaros modeling, based on functional neuroimaging studies and previous neuroanatomical data from animal models, to probe the connectivity of brain systems involved in stressor-evoked cardiovascular reactivity and to explore TMS potential as a tool for detection and stratification of individual differences concerning this reactivity and hemorreological risk factors correlated with the development of Coronary Heart Disease (CHD). Methods: Both subjects, a 52 years old male and a 40 years old female with previous increased Low Frequency (LF)/High Frequency (HF) Heart Rate Variability (HRV) ratios (respectively, 4.209/3.028) without decompensated cardiorespiratory symptoms, gave informed consent, and ethico-legal issues have been observed. Electroencephalographic (EEG) monitoring has been performed for safety purposes. Immediately after administration, over the mPFC, of 15 pulses of rTMS, during 60 second, with an inductive electrical current, at the stimulating coil, of 85.9 Ampère per μsecond and 66 Ampère per μsecond, respectively, for male and female subjects (a “figure-of-eight” coil and magnetic stimulator MagLite, Dantec/Medtronic, have been used), HRV spectrum analysis (cStress software) has been performed (during 5 minutes, in supine position). Results: In both subjects, LF power, HF power and LF/HF ratio results, before and after rTMS administration, pointed towards sympathetic attenuation and parasympathetic augmentation (respectively, in male/female subject: decreased LF power—65.1 nu/69.3 nu, before rTMS; 56.1 nu/41.6 nu, after rTMS; increased HF power—15.5 nu/22.9 nu, before rTMS; 30.9 nu/45.5 nu, after rTMS). Conclusions: In this preliminary investigation, the existence of a link between “mind” and heart’s function has been put in evidence, through a reversible “virtual” lesion, of brain systems involved in cardiovascular control, caused by TMS. Repetitive TMS over mPFC decreased brain function involved in stressorevoked cardiovascular reactivity, suggesting the importance of TMS in the management of stress-related cardiovascular disorders.

Influência da cafeína na resposta pressórica ao exercício aeróbio em sujeitos hipertensos

A redução da pressão arterial (PA) promovida pelo exercício físico é evidente segundo a literatura atual. Mecanismos neuro-humorais explicam essa resposta hipotensora, em que a diminuição da atividade simpática apresenta-se como um dos principais mecanismos. Porém, a ingestão de alimentos ricos em cafeína (CA) pode suprimir esta atenuação simpática. O objetivo desse estudo foi elucidar o impacto da ingestão de CA na resposta pressórica ao exercício em pessoas hipertensas. Sete hipertensos (52,3 ± 3,3 anos), sendo cinco mulheres, realizaram duas sessões de caminhada com 40 minutos de duração, em dois dias de treinamento, tendo previamente ingerido CA (4mg/kg de peso corporal) ou placebo (PL). A PA e a frequência cardíaca foram verificadas anteriormente a ingestão, após 15, 30, 45, 60 minutos da ingestão em estado de repouso e com 10, 20 e 30 minutos após o exercício. Os dados foram tratados por meio de estatística descritiva, e pelo teste não paramétrico de Wilcoxon (p &lt; 0,05). A média da PA aumentou de 124,9/80,9mmHg antes da ingestão de CA para 129,4/84,3mmHg 60 minutos após, ainda no repouso (p &lt; 0,05). Trinta minutos após o exercício observou-se resposta hipotensora no procedimento PL (queda da PA de 122,6/79,4mmHg para 115,7/78,6mmHg), enquanto que no procedimento com CA, a PA mostrou-se significativamente mais alta em relação aos valores de repouso (aumento de 124,9/80,9mmHg para 136,9/90,9mmHg, p &lt; 0,05). Conclui-se que a ingestão de CA não só suprime a resposta hipotensora do exercício, como provoca uma hipertensão pós-exercício.

State-of-the-Art lecture: influence of exercise training on neurogenic control of blood pressure in spontaneously hypertensive rats.

Exercise training plays an important role in the reduction of high blood pressure. In this review, we discuss the effect of distinct intensities of exercise training on the reduction of high blood pressure in spontaneously hypertensive rats (SHR). In addition, we present some hemodynamic mechanisms and associated neural controls by which exercise training attenuates hypertension in SHR. Low-intensity exercise training is more effective in reducing high blood pressure than is high-intensity exercise training in SHR. The decrease in blood pressure is due to resting bradycardia, and in consequence, lower cardiac output. Sympathetic attenuation to the heart is the major explanation for the resting bradycardia. Recovery of the sensitivity of baroreflex control of heart rate, which is usually impaired in SHR, is an important neurogenic component involved in the benefits elicited by exercise training.

Escape of parasympathetic vasodilatation from sympathetic attenuation in oro-facial areas in the cat.

We examined the effects of concurrent repetitive stimulation of the cervical sympathetic trunk (CST) on the parasympathetically mediated reflex blood flow increase in the orofacial area of cats. In urethane plus alpha-chloralose anaesthetized cats, parasympathetic reflex vasodilatation in the ipsilateral lower lip was elicited by electrical stimulation of the central cut end of the lingual nerve (LN). This blood flow increase was attenuated in a frequency-dependent manner when CST was stimulated concurrently at 0.5-10 Hz for 10 minutes. When we applied repeated LN stimulation (using identical parameters, each time) at intervals during a 30-minutes period of 10 Hz CST stimulation, the attenuation of the blood flow increase gradually weakened in a time-dependent manner even though the direct vasoconstrictor effect of CST stimulation showed no such decline.

Sympathetic attenuation of parasympathetic vasodilatation in oro‐facial areas in the cat

1. The present study was designed to examine the interaction between sympathetic and parasympathetic influences on blood flow in oro-facial areas such as lower lip, palate and submandibular gland (SMG) and in the common carotid artery (CCA) in anaesthetized cats. 2. Section of the ipsilateral superior cervical sympathetic trunk (CST) increased the basal CCA blood flow significantly. The control level with the nerve intact was comparable with that seen at 0.5-1 Hz CST stimulation, suggesting a spontaneous discharge of around 0. 5-1 Hz in the CST fibres innervating the beds supplied by the CCA. The basal blood flow at all sites examined was reduced by CST stimulation in a frequency-dependent manner. 3. Electrical stimulation of the central end of the lingual nerve (LN) evoked blood flow increases in the lower lip and palate. These blood flow increases were markedly reduced by concurrent CST stimulation in a manner that was frequency dependent, but not simply related to the vasoconstrictor effect of CST stimulation. This effect of CST stimulation was not observed in tongue or SMG, even though CST stimulation evoked vasoconstriction in these tissues. A significant reduction in the level of CCA blood flow attained during LN stimulation was observed on repetitive CST stimulation only at 10 Hz, indicating that this response behaved in a fashion different from that seen in the lower lip, palate, tongue and SMG. 4. The present study suggests that concurrent repetitive CST stimulation reduces parasympathetically mediated blood flow increases in certain oro-facial areas (such as the lower lip and palate), but not in the tongue and SMG. This inhibitory action was not a simple additive effect (between vasoconstriction and vasodilatation) and it disappeared rapidly after the cessation of CST stimulation.

Glibenclamide enhances but pinacidil reduces attenuation in sympathetic responsiveness after acute coronary artery occlusion.

To investigate the role of ATP-sensitive K+ channels in modulating the efferent autonomic response following acute myocardial ischemia/infarction, we examined the effects of a blocker (glibenclamide) and an opener (pinacidil) of ATP-sensitive K+ channels on the time course and extent of the attenuation in efferent cardiac sympathetic responsiveness in anesthetized dogs. We measured the effective refractory periods (ERPs) at nonischemic sites basal and apical to the area of myocardial ischemia/infarction in the baseline state and during bilateral stimulation of the ansae subclaviae before and after each drug administration and 5, 30, 60, 120, and 180 minutes after latex injection of a diagonal branch of the left anterior descending coronary artery. Animals received either vehicle (n = 12), glibenclamide (0.3 mg.kg-1, n = 10), pinacidil (0.15 mg.kg-1 + 0.2 mg.kg-1 infusion, n = 10), or a combination of these two drugs (n = 9) intravenously. In another group of dogs receiving just pinacidil (n = 10), an intra-aortic balloon was inflated distal to the renal arteries to prevent pinacidil-induced hypotension. Another group of dogs received either high-dose glibenclamide (0.3 mg.kg-1 + 0.15 mg.kg-1, n = 4), low-dose glibenclamide (0.06 mg.kg-1, n = 4), medium-dose pinacidil (0.03 mg.kg-1 + 0.04 mg.kg-1 infusion, n = 4), or low-dose pinacidil (0.0075 mg.kg-1 + 0.01 mg.kg-1 infusion, n = 4). In all dogs, basal sites exhibited no attenuation of sympathetically induced shortening of the ERP throughout the period of acute myocardial ischemia/infarction. Cumulative attenuation in sympathetic responsiveness (shortening of ERP < or = 2 milliseconds induced by bilateral stimulation of the ansae subclaviae) at nonischemic test sites apical to the area of ischemia/infarction during a 3-hour period was greater in the glibenclamide group (26 of 44 sites, P = .008) and less in the pinacidil (2 of 44 sites, P = .002) and pinacidil-balloon (1 of 48 sites, P < .001) groups compared with the vehicle group (14 of 46 sites). Glibenclamide abolished the protective effect of pinacidil so that 10 of 45 sites had < 2-millisecond shortening during a 3-hour period in the glibenclamide + pinacidil group (P = .018 versus pinacidil group, P = .286 versus vehicle group). Such effects of glibenclamide and pinacidil on sympathetic attenuation were dose dependent. Maintaining the blood glucose level during glibenclamide administration did not affect the sympathetic attenuation after acute coronary artery occlusion.(ABSTRACT TRUNCATED AT 400 WORDS)

Defibrillating shocks delivered to the heart impair efferent sympathetic responsiveness.

Functional studies indicate that sympathetic efferents are located in the superficial subepicardium and vagal efferents are located in the subendocardium. It is possible that electrical shocks applied directly to the heart might affect the function of these autonomic nerves. Low- (< or = 1 J), medium- (6 to 16 J), or high- (30 to 35 J) energy truncated monophasic exponential shocks, synchronized to the R wave during sinus rhythm, were delivered over implantable patches sutured inside the pericardium in anesthetized open-chest dogs. Shortening of ventricular effective refractory period (ERP), produced by bilateral ansae subclaviae stimulation (SS), was measured before and after shock delivery. High-energy shocks shifted the SS frequency-ERP response curves downward and to the right (P < .001) for sites beneath and apical to the patches; ERP shortening at basal sites remained unchanged. Such sympathetic attenuation occurred with shocks > 10 J but not with shocks < or = 10 J, was noted 15 minutes after the shock, and showed incomplete return to control values at 3 hours. Neither low- nor high-energy shocks affected norepinephrine dose-ERP response curves, indicating normal myocardial responsiveness. Low- and high-energy shocks did not attenuate bilateral cervical vagal stimulation-induced ERP prolongation. High-energy shocks delivered over patches sutured to the outside of the pericardium showed no effects on sympathetic response, suggesting a protective effect of the pericardium against shock-induced sympathetic attenuation. DC shocks > 10 J delivered directly to the epicardium attenuated efferent sympathetic neural function. Such changes may affect electrophysiological, as well as hemodynamic, responses to sympathetic neural stimulation after cardioversion-defibrillation.