The bed nucleus of the stria terminalis modulates exercise-evoked cardiovascular responses in rats

Dynamic exercise evokes sustained cardiovascular changes, which are characterized by blood pressure and heart rate (HR) increases. Although it is well accepted that there is a central nervous system (CNS) mediation of cardiovascular adjustments during dynamic exercise, information on the role of specific CNS structures is limited. The bed nucleus of the stria terminalis (BST) is a forebrain structure known to be involved in central cardiovascular control. Based on this, we tested the hypothesis that BST modulates HR and mean arterial pressure (MAP) responses evoked when rats are submitted to dynamic exercise. Male Wistar rats were tested at three levels of exercise (0.4, 0.8 and 1 km h-1) on a rodent treadmill before and after BST treatment with CoCl(2), a non-selective neurotransmission blocker. Bilateral microinjection of CoCl(2) (1 nmol in 100 nl artificial cerebrospinal fluid) into the BST reduced the pressor response to exercise at 0.4 km h-1 as well as the tachycardic responses evoked by exercise at 0.4, 0.8 and 1 km h-1. The BST treatment with CoCl(2) did not affect baseline MAP or HR, suggesting a lack of tonic BST influence on cardiovascular parameters at rest. Moreover, BST treatment with CoCl(2) did not affect motor performance in the open-field test, which indicates that effects of BST inhibition on cardiovascular responses to dynamic exercise are not due to changes in motor activity. The present results suggest that local neurotransmission in the BST modulates exercise-related cardiovascular adjustments. Data indicate that BST facilitates pressor and tachycardic responses evoked by dynamic exercise in rats.

Effect of acute restraint stress on the tachycardiac and bradycardiac responses of the baroreflex in rats

In the present study, we evaluated cardiac baroreflex responses of rats submitted to acute restraint stress. The baroreflex was tested: immediately before, during a 30 min exposure to restraint stress, as well as 30 and 60 min after ending the stress session (recovery period). Restraint increased both mean arterial pressure (MAP) and heart rate (HR). The magnitude of tachycardiac responses evoked by intravenous infusion of sodium nitroprusside was higher during restraint stress, whereas that of bradycardiac responses evoked by intravenous infusion of phenylephrine was decreased. Restraint-evoked baroreflex changes were still observed at 30 min into the recovery period, although MAP and HR values had already returned to control values. The baroreflex was back to control values at 60 min of the recovery period. Intravenous administration of the selective beta(1)-adrenoceptor antagonist atenolol blocked the restraint-evoked increase in the tachycardiac baroreflex response, but did not affect the effects on the bradycardiac response. In conclusion, the present results suggest that psychological stresses, such as those resulting from acute restraint, affect the baroreflex. Restraint facilitated the tachycardiac baroreflex response and reduced the bradycardiac response. Restraint-related effects on baroreflex persisted for at least 30 min after ending restraint, although MAP and HR had already returned to control levels. The cardiac baroreflex returned to control values 60 min after the end of restraint, indicating non-persistent effects of acute restraint on the baroreflex. Results also indicate that the influence of restraint stress on the baroreflex tachycardiac response is mainly dependent on cardiac sympathetic activity, whereas the action on the bradycardiac response is mediated by the cardiac parasympathetic component.

Cardiovascular effects of noradrenaline microinjection into the medial part of the superior colliculus of unanesthetized rats

The superior colliculus (SC) is a mesencephalic area involved in the mediation of defensive movements associated with cardiovascular changes. Noradrenaline (NA) is a neurotransmitter with an important role in central cardiovascular regulation exerted by several structures of the central nervous system. Although noradrenergic nerve terminals have been observed in the SC, there are no reports on the effects of local NA injection into this area. Taking this into consideration, we studied the cardiovascular effects of NA microinjection into the SC of unanesthetized rats. Microinjection of NA into the SC evoked a dose-dependent blood pressure increase and a heart rate decrease in unanesthetized rats. The pressor response to NA was not modified by intravenous pretreatment with the vasopressin v(1)-receptor antagonist dTyr(CH(2))(5) (Me)AVP, indicating a lack of vasopressin involvement in the response mediation. The effect of NA microinjection into the SC was blocked by intravenous pretreatment with the ganglionic blocker pentolinium, indicating its mediation by the sympathetic nervous system. Although the pressor response to NA was not affected by adrenal demedullation, the accompanying bradycardia was potentiated, suggesting some involvement of the sympathoadrenal system in the cardiovascular response to NA microinjection into the SC. In summary, results indicate that stimulation of noradrenergic receptors in the SC causes cardiovascular responses which are mediated by activation of both neural and adrenal sympathetic nervous system components. (C) 2009 Elsevier B.V. All rights reserved.

Day-night pattern of autonomic nervous system modulation in patients with heart failure with and without sleep apnea

Introduction: Among patients with congestive heart failure (CHF) both obstructive and central sleep apnea (SA) are associated with increased sympathetic activity. However, the day-night pattern of cardiac autonomic nervous system modulation in CHF patients with and without sleep apnea is unknown. Material and methods: Twenty-five CHF patients underwent polysomnography with simultaneous beat-to-beat blood pressure (Portapres), respiration and electrocardiogram monitoring. Patients were divided according to the presence (SA, n=17) and absence of SA (NoSA, n=8). Power spectral analyses of heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS) were determined in periods with stable breathing while awake at 6 AM, 10 AM, 10 PM, as well as during stage 2 sleep. In addition, muscle sympathetic nerve activity (MSNA) was evaluated at 10 AM. Results: RR variance, low-frequency (LF), high-frequency (HF) powers of HRV, and BRS were significantly lower in patients with SA compared with NoSA in all periods. HF power, a marker of vagal activity, increased during sleep in patients with NoSA but in contrast did not change across the 24-hour period in patients with SA. MSNA was significantly higher in patients with SA compared with NoSA. RR variance, LF and HF powers correlated inversely with simultaneous MSNA (r=-0.64, -0.61, and -0.61 respectively; P < 0.01). Conclusions: Patients with CHF and SA present a reduced and blunted cardiac autonomic modulation across the 24-hour period. These findings may help to explain the increased cardiovascular risk in patients with CHF and SA. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Dopamine microinjected into brainstem of awake rats affects baseline arterial pressure but not chemoreflex responses

Dopamine (DA) is a neuromodulator in the brainstem involved with the generation and modulation of the autonomic and respiratory activities. Here we evaluated the effect of microinjection of DA intracistema magna (icm) or into the caudal nucleus tractus solitarii (cNTS) on the baseline cardiovascular and respiratory parameters and on the cardiovascular and respiratory responses to chemoreflex activation in awake rats. Guide cannulas were implanted in cisterna magna or cNTS and femoral artery and vein were catheterized. Respiratory frequency (f(R)) was measured by whole-body plethysmography. Chemoreflex was activated with KCN (iv) before and after microinjection of DA icm or into the cNTS bilaterally while mean arterial pressure (MAP), heart rate (HR) and f(R) were recorded. Microinjection of DA icm (n = 13), but not into the cNTS (n = 8) produced a significant decrease in baseline MAP (-15 +/- 1 vs 1 +/- 1 mm Hg) and HR (-55 +/- 11 vs -11 +/- 17 bpm) in relation to control (saline with ascorbic acid, n = 9) but no significant changes in baseline f(R). Microinjection of DA icm or into the cNTS produced no significant changes in the pressor, bradycardic and tachypneic responses to chemoreflex activation. These data show that a) DA icm affects baseline cardiovascular regulation, but not baseline f(R) and autonomic and respiratory components of chemoreflex and b) DA into the cNTS does not affect either the autonomic activity to the cardiovascular system or the autonomic and respiratory responses of chemoreflex activation. (C) 2010 Elsevier B.V. All rights reserved.

GABA and nitric oxide in the PVN are involved in arterial pressure control but not in the chemoreflex responses in rats

GABAergic, nitrergic and glutamatergic mechanisms in the PVN on the baseline mean arterial pressure (MAP), heart rate (HR) and on the cardiovascular responses to chemoreflex activation in awake rat were evaluated. Chemoreflex was activated with KCN before and after microinjections into the PVN. Bicuculline into the PVN increased baseline MAP (94+/-3 vs 113+/-5 mmHg) and HR (350+/-9 vs 439+/-18 bpm) but had no effect on the pressor (49+/-5 vs 47+/-6 mmHg) or bradicardic (-213+/-23 vs -256+/-42 bpm) responses (n=7). Kynurenic acid into the PVN (n=6) produced no significant changes in the MAP (98+/-3 vs 100+/-3 mmHg), HR (330+/-5 vs 339+/-12 mmHg) or in the pressor (50+/-4 vs 42+/-4 mmHg) and bradicardic (-252+/-4 vs -285+/-16 bpm) responses to chemoreflex. L-NAME into the PVN (n=8) produced increase in the MAP (94+/-3 vs 113+/-5 mmHg) and HR (350+/-9 vs 439+/-18 bpm) but had no effect on the pressor (52+/-5 vs 47+/-6 mmHg) or bradicardic (-253+/-19 vs -320+/-25 bpm) responses to chemoreflex. We conclude that GABA(A) and nitric oxide in the PVN are involved in the maintenance of the baseline MAP but not in the modulation of the responses to chemoreflex. The results also show that Glutamate receptors in the PVN are not involved in maintenance of the baseline MAP, HR or in the cardiovascular responses to chemoreflex in awake rats. (C) 2008 Elsevier B.V. All rights reserved.

Increased cardiac sympathetic drive and reduced vagal modulation following endothelin receptor antagonism in healthy conscious rats

1. The present study evaluated changes in autonomic control of the cardiovascular system in conscious rats following blockade of endothelin (ET) receptors with bosentan. 2. Rats were treated with bosentan or vehicle (5% gum arabic) for 7 days by gavage. 3. Baseline heart rate (HR) was higher in the bosentan-treated group compared with the control group (418 +/- 5 vs 357 +/- 4 b.p.m., respectively; P < 0.001). This baseline tachycardia was associated with a lower baroreflex sensitivity of the bradycardiac and tachycardiac responses in the bosentan-treated group compared with the control group. Sequential blockade of the parasympathetic and sympathetic autonomic nervous system with methylatropine and propranolol showed a higher intrinsic HR in the bosentan-treated group compared with the control group (411 +/- 5 vs 381 +/- 4 b.p.m., respectively; P < 0.05). This was accompanied by a higher cardiac sympathetic tone (31 +/- 1 vs 13 +/- 1%, respectively; P < 0.01) and a lower vagal parasympathetic tone (69 +/- 2 vs 87 +/- 2%, respectively; P < 0.01) in the bosentan-treated group compared with the control group. Variance and high-frequency oscillations of pulse interval (PI) variability in absolute and normalized units were lower in the bosentan-treated group than in the control group. Conversely, low-frequency (LF) oscillations of PI variability in absolute and normalized units, as well as variance and LF oscillations of systolic arterial pressure variability, were greater in the bosentan-treated group than the control group. 4. Overall, the data indicate an increased cardiac sympathetic drive, as well as lower vagal parasympathetic activity and baroreflex sensitivity, in conscious rats after chronic blockade of ET receptors with bosentan.

Cardiopulmonary and isoflurane-sparing effects of epidural or intravenous infusion of dexmedetomidine in cats undergoing surgery with epidural lidocaine

Objective To compare the cardiorespiratory, anesthetic-sparing effects and quality of anesthetic recovery after epidural and constant rate intravenous (IV) infusion of dexmedetomidine (DEX) in cats given a low dose of epidural lidocaine under propofol-isoflurane anesthesia and submitted to elective ovariohysterectomy. Study design Randomized, blinded clinical trial. Animals Twenty-one adult female cats ( mean body weight: 3.1 +/- 0.4 kg). Methods Cats received DEX (4 mu g kg(-1), IM). Fifteen minutes later, anesthesia was induced with propofol and maintained with isoflurane. Cats were divided into three groups. In GI cats received epidural lidocaine (1 mg kg(-1), n = 7), in GII cats were given epidural lidocaine (1 mg kg(-1)) + DEX (4 mu g kg(-1), n = 7), and in GIII cats were given epidural lidocaine (1 mg kg(-1)) + IV constant rate infusion (CRI) of DEX (0.25 mu g kg(-1) minute(-1), n = 7). Variables evaluated included heart rate (HR), respiratory rate (f(R)), systemic arterial pressures, rectal temperature (RT), end-tidal CO(2), end-tidal isoflurane concentration (E`ISO), arterial blood gases, and muscle tone. Anesthetic recovery was compared among groups by evaluation of times to recovery, HR, f(R), RT, and degree of analgesia. A paired t-test was used to evaluate pre-medication variables and blood gases within groups. ANOVA was used to compare parametric data, whereas Friedman test was used to compare muscle relaxation. Results Epidural and CRI of DEX reduced HR during anesthesia maintenance. Mean +/- SD E/ISO ranged from 0.86 +/- 0.28% to 1.91 +/- 0.63% in GI, from 0.70 +/- 0.12% to 0.97 +/- 0.20% in GII, and from 0.69 +/- 0.12% to 1.17 +/- 0.25% in GIII. Cats in GII and GIII had longer recovery periods than in GI. Conclusions and clinical relevance Epidural and CRI of DEX significantly decreased isoflurane consumption and resulted in recovery of better quality and longer duration, despite bradycardia, without changes in systemic blood pressure.

Peripartum Haemodynamic Status of Bitches with Normal Birth or Dystocia

There has been limited investigation of parturition in the bitch and there is little information published on clinical and obstetrical examination other than opinion and anecdote. While there are substantial data on haemodynamic and vascular changes during normal parturition in humans, little is known about the physiological events in the dog. This study was aimed at maternal haemodynamic changes occurring during normal parturition and to investigate how these were modified in bitches with dystocia (DYST) treated either medically or via assisted delivery and caesarean operation. Three groups of 10 bitches were investigated; those with normal parturition, those with DYST corrected by manipulative assistance or caesarean operation and those with uterine inertia treated by oxytocin administration. Heart rate, systolic and diastolic blood pressure, electrocardiogram and blood glucose concentration were measured pre-partum, intra-partum, immediately after parturition and 1 h later. Heart rate was high at all times throughout the study and the majority of bitches had normal sinus rhythm. Blood pressure was generally within the normal range, and although systolic and diastolic blood pressure was highest during the intra-partum period and sometimes during the immediate post-partum period, there were no significant differences between groups. All bitches had blood glucose concentrations within the normal range throughout the study although pre-partum concentrations were statistically lower than many of the other time periods. The study provides useful physiological data that will facilitate monitoring and clinical management of bitches throughout normal parturition and DYST.

Role of central nitric oxide in behavioral thermoregulation of toads during hypoxia

Nitric oxide (NO) is thought to play a key role in the development of hypoxia-induced anapyrexia in mammals, acting on the preoptic region of the anterior hypothalamus to activate autonomic heat loss responses. Regarding behavioral thermoregulation, no data exists for NO modulation/mediation of thermoregulatory behavior changes during hypoxia. Therefore, we tested the hypothesis that NO is involved in the preferred body temperature (Tb) reduction in the hypoxic toad Chaunus schneideri (formerly Bufo paracnemis), a primarily behavioral thermoregulator. Toads equipped with a temperature probe were placed in a thermal gradient chamber, and preferred Tb was monitored continuously. We analyzed the effect of intracerebroventricular injections of the nonselective NO synthase inhibitor L-NMMA (200, 400 and 800 microg per animal) or mock cerebrospinal fluid (mCSF, vehicle) on the preferred Tb of toads. No significant difference in preferred Tb was observed after L-NMMA treatments. Another group of toads treated with 2 mg kg(-1) (400 microg per animal) of L-NMMA or mCSF was submitted to hypoxia (3% inspired 02) for 8 h. The vehicle group showed a reduction of preferred Tb, a response that was inhibited by L-NMMA. A 3rd group of hypoxic animals was injected with Ringer or L-NMMA (2 mg kg(-1)) into the lymph sac and both treatments induced no change in the anapyretic response to hypoxia. These results indicate that NO acting on the central nervous system has an excitatory role for the development of hypoxia-induced anapyrexia in toads. (C) 2008 Elsevier Inc. All rights reserved.

Effects of physiotherapy on hemodynamic variables in newborns with Acute Respiratory Distress Syndrome

Background: Acute respiratory distress syndrome (ARDS) is a frequent respiratory disturbance in preterm newborns. Preceding investigations evaluated chronic physiotherapy effects on newborns with different lung diseases; however, no study analyzed acute physiotherapy treatment on premature newborns with ARDS. In this study we aimed to evaluate the acute effects of chest and motor physiotherapy treatment on hemodynamic variables in preterm newborns with ARDS. Methods: We evaluated heart rate (HR), respiratory rate (RR), systolic (SAP), mean (MAP) and diastolic arterial pressure (DAP), temperature and oxygen saturation (SO(2)%) in 44 newborns with ARDS. We compared all variables between six periods in one day: before first physiotherapy treatment vs. after first physiotherapy treatment vs. before second physiotherapy treatment vs. after second physiotherapy treatment vs. before third physiotherapy treatment vs. after third physiotherapy treatment. Variables were measured 2 minutes before and 5 minutes after each physiotherapy session. We applied Anova one way followed by post hoc Bonferroni test. Results: HR (147.5 +/- 9.5 bpm vs. 137.7 +/- 9.3 bpm; p<0.001), RR (45.5 +/- 8.7cpm vs. 41.5 +/- 6.7 cpm; p=0.001), SAP (70.3 +/- 10.4 mmHg vs. 60.1 +/- 7.1 mmHg; p=0.001) and MAP (55.7 +/- 10 mmHg vs. 46 +/- 6.6 mmHg; p=0.001) were significantly reduced after the third physiotherapy treatment compared to before the first session. There were no significant changes regarding temperature, DAP and SO(2) %. Conclusion: Chest and motor physiotherapy acutely improves HR, RR, SAP, MAP and SO(2) % in newborns with ARDS.

Cardiovascular and autonomic phenotype of db/db diabetic mice

The db/db mice serve as a good model for type 2 diabetes characterized by hyperinsulinaemia and progressive hyperglycaemia. There are limited and conflicting data on the cardiovascular changes in this model. The aim of the present study was to characterize the cardiovascular and autonomic phenotype of male db/db mice and evaluate the role of angiotensin II AT(1) receptors. Radiotelemetry was used to monitor 24 h blood pressure (BP) in mice for 8 weeks. Parameters measured were mean arterial pressure (MAP), heart rate (HR) and their variabilities. In 8-week-old db/db mice, the MAP and BP circadian rhythms were not different from age-matched control mice, while HR and locomotor activity were decreased. With ageing, MAP gradually increased in db/db mice, and the 12 h light values did not dip significantly from the 12 h dark periods. In 14-week-old mice, MAP was increased during light (101 +/- 1 versus 117 +/- 2 mmHg, P < 0.01; control versus db/db mice) and dark phases (110 +/- 1.7 versus 121 +/- 3.1 mmHg, P < 0.01; control versus db/db mice). This increase in MAP was associated with a significant increase in plasma angiotensin-converting enzyme activity and angiotensin II levels. Chronic treatment with losartan (10 mg kg(-1) day(-1)) blocked the increase in MAP in db/db mice, with no effect in control animals. Spectral analysis was used to monitor autonomic cardiovascular function. The circadian rhythm observed in systolic arterial pressure variance and its low-frequency component in control mice was absent in db/db mice. There were no changes in HR variability and spontaneous baroreflex sensitivity between control and db/db mice. The results document an age-related increase in MAP in db/db mice, which can be reduced by antagonism of angiotensin II AT(1) receptors, and alterations in autonomic balance and components of the renin-angiotensin system.

Exercise improves cardiovascular control in a model of dislipidemia and menopause

The present study investigated the effects of exercise training on arterial pressure, baroreflex sensitivity, cardiovascular autonomic control and metabolic parameters on female LDL-receptor knockout ovariectomized mice. Mice were divided into two groups: sedentary and trained. Trained group was submitted to an exercise training protocol. Blood cholesterol was measured. Arterial pressure (AP) signals were directly recorded in conscious mice. Baroreflex sensitivity was evaluated by tachycardic and bradycardic responses to AP changes. Cardiovascular autonomic modulation was measured in frequency (FFT) and time domains. Maximal exercise capacity was increased in trained as compared to sedentary group. Blood cholesterol was diminished in trained mice (191 +/- 8 mg/dL) when compared to sedentary mice (250 +/- 9 mg/dL, p<0.05). Mean AP and HR were reduced in trained group (101 +/- 3 mmHg and 535 +/- 14 bpm, p<0.05) when compared with sedentary group (125 +/- 3 mmHg and 600 +/- 12 bpm). Exercise training induced improvement in bradycardic reflex response in trained animals (-4.24 +/- 0.62 bpm/mmHg) in relation to sedentary animals (-1.49 +/- 0.15 bpm/mmHg, p<0.01); tachycardic reflex responses were similar between studied groups. Exercise training increased the variance (34 +/- 8 vs. 6.6 +/- 1.5 ms(2) in sedentary, p<0.005) and the high-frequency band (HF) of the pulse interval (IP) (53 +/- 7% vs. 26 +/- 6% in sedentary, p<0.01). It is tempting to speculate that results of this experimental study might represent a rationale for this non-pharmacological intervention in the management of cardiovascular risk factors in dyslipidemic post-menopause women. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

HISTAMINE IN THE POSTERODORSAL MEDIAL AMYGDALA MODULATES CARDIOVASCULAR REFLEX RESPONSES IN AWAKE RATS

Centrally injected histamine (HA) affects heart rate (HR), arterial blood pressure (BP), and sympathetic activity in rats. The posterodorsal medial amygdala (MePD) has high levels of histidine decarboxylase, connections with brain areas involved with the modulation of cardiovascular responses, and is relevant for the pathogenesis of hypertension. However, there is no report demonstrating the role of the MePD histaminergic activity on the cardiovascular function in awake rats. The alms of the present work were: 1) to study the effects of two doses (10-100 nM) of HA microinjected in the MePD on basal cardiovascular recordings and on baroreflex- and chemoreflex-mediated responses; 2) to reveal whether cardiovascular reflex responses could be affected by MePD microinjections of (R)-alpha-methylhistamine (AH(3)), an agonist of the inhibitory autoreceptor H(3); and, 3) to carry out a power spectral analysis to evaluate the contribution of the sympathetic and parasympathetic components in the variability of the HR and BP recordings. When compared with the control group (microinjected with saline, 0.3 mu l), HA (10 nM) promoted an increase in the MAP(50), i.e. the mean value of BP at half of the HR range evoked by the baroreflex response. Histamine (100 nM) did not affect the baroreflex activity, but significantly decreased the parasympathetic component of the HR variability, increased the sympathetic/parasympathetic balance at basal conditions (these two latter evaluated by the power spectral analysis), and promoted an impairment in the chemoreflex bradycardic response. Microinjection of AH(3) (10 mu M) led to mixed results, which resembled the effects of both doses of HA employed here. Present data suggest that cardiovascular changes induced by baroreceptors and chemoreceptors involve the histaminergic activity in the MePD. This neural regulation of reflex cardiovascular responses can have important implications for homeostatic and allostatic conditions and possibly for the behavioral displays modulated by the rat MePD. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.

Effects of exercise training on autonomic dysfunction management in an experimental model of menopause and myocardial infarction

Objective: The aim of this study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction in ovariectomized rats submitted to myocardial infarction. Methods: Female Wistar rats were divided into the following ovariectomized groups: sedentary ovariectomized (SO), trained ovariectomized (TO), sedentary ovariectomized infarcted (SOI), and trained ovariectomized infarcted (TOI). Trained groups were submitted to an exercise training protocol on a treadmill (8 wk). Arterial baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes, and cardiopulmonary baroreflex sensitivity was tested by bradycardic and hypotension responses to serotonin injection. Vagal and sympathetic effects were calculated by pharmacological blockade. Results: Arterial pressure was reduced in the TO in comparison with the SO group and increased in the TOI in relation to the SOI group. Exercise training improved the baroreflex sensitivity in both the TO and TOI groups. The TOI group displayed improvement in cardiopulmonary reflex sensitivity compared with the SOI group at the 16 mu g/kg serotonin dose. Exercise training enhanced the vagal effect in both the TO (45%) and TOI (46%) animals compared with the SO and SOI animals and reduced the sympathetic effect in the TOI (38%) in comparison with the SOI animals. Significant correlations were obtained between bradycardic baroreflex responses and vagal (r = -0.7, P < 0.005) and sympathetic (r = 0.7, P < 0.001) effects. Conclusions: These results indicate that exercise training in ovariectomized rats submitted to myocardial infarction improves resting hemodynamic status and reflex control of the circulation, which may be due to an increase in the vagal component. This suggests a homeostatic role for exercise training in reducing the autonomic impairment of myocardial infarction in postmenopausal women.