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This study investigated the role of AT 1 , AT 2 and Mas angiotensinergic receptors within the MeA in autonomic, cardiovascular and baroreflex changes evoked by a 10-day (1  hr daily) repeated restraint stress (RRS) protocol. Analysis of cardiovascular function after the end of the RRS protocol indicated increased values of arterial pressure, without heart rate changes. Arterial pressure increase was not affected by acute MeA treatment after the RRS with either the selective AT 1 receptor antagonist losartan, the selective AT 2 receptor antagonist PD123319 or the selective Mas receptor antagonist A-779. Analysis of heart rate variability indicated that RRS increased the sympathetic tone to the heart, which was inhibited by MeA treatment with either losartan, PD123319 or A-779. Baroreflex function assessed using the pharmacological approach via intravenous infusion of vasoactive agents revealed a facilitation of tachycardia evoked by blood pressure decrease in chronically stressed animals, which was inhibited by MeA treatment with losartan. Conversely, baroreflex responses during spontaneous fluctuations of blood pressure were impaired by RRS, and this effect was not affected by injection of the angiotensinergic receptor antagonists into the MeA. Altogether, the data reported in the present study suggest an involvement of both angiotensinergic receptors present in the MeA in autonomic imbalance evoked by RRS, as well as an involvement of MeA AT 1 receptor in the enhanced baroreflex responses during full range of blood pressure changes. Results also indicate that RRS-evoked increase in arterial pressure and impairment of baroreflex responses during spontaneous variations of arterial pressure are independent of MeA angiotensinergic receptors., (© 2020 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

Surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI) are options in severe aortic valve stenosis (AVS). Cardiovascular (CV) and cerebrovascular (CBV) control markers, derived from variability of heart period, systolic arterial pressure, mean cerebral blood velocity and mean arterial pressure, were acquired in 19 AVS patients (age: 76.8 ± 3.1 yrs, eight males) scheduled for SAVR and in 19 AVS patients (age: 79.9 + 6.5 yrs, 11 males) scheduled for TAVI before (PRE) and after intervention (POST, <7 days). Left ventricular function was preserved in both groups. Patients were studied at supine resting (REST) and during active standing (STAND). We found that: (i) both SAVR and TAVI groups featured a weak pre‐procedure CV control; (ii) TAVI ensured better CV control; (iii) cerebral autoregulation was working in PRE in both SAVR and TAVI groups; (iv) SAVR and TAVI had no impact on the CBV control; (v) regardless of group, CV and CBV control markers were not influenced by STAND in POST. Even though the post‐procedure preservation of both CV and CBV controls in TAVI group might lead to privilege this procedure in patients at higher risk, the missing response to STAND suggests that this advantage could be insignificant. [ABSTRACT FROM AUTHOR]

Dysregulation of cardiovascular autonomic control is gaining recognition as a prevailing consequence of concussion injury. Characterizing the presence of autonomic dysfunction in concussed persons is inconsistent and conventional metrics of autonomic function cannot differentiate the presence/absence of injury. Mayer wave (MW) activity originates through baroreflex adjustments to blood pressure (BP) oscillations that appear in the low‐frequency (LF: 0.04–0.15 Hz) band of the BP and heart rate (HR) power spectrum after a fast Fourier transform. We prospectively explored MW activity (∼0.1 Hz) in 19 concussed and 19 noninjured athletes for 5 min while seated at rest within 48 h and 1 week of injury. MW activity was derived from the LF band of continuous digital electrocardiogram and beat‐to‐beat BP signals (LFHR, LF‐SBP, MWHR, and MW‐SBP, respectively); a proportion between MWBP and MWHR was computed (cMW). At 48 h, the concussion group had a significantly lower MWBP and cMW than controls; these differences were gone by 1 week. MWHR, LFHR, and LF‐SBP were not different between groups at either visit. Attenuated sympathetic vasomotor tone was present and the central autonomic mechanisms regulating MW activity to the heart and peripheral vasculature became transiently discordant early after concussion with apparent resolution by 1 week. [ABSTRACT FROM AUTHOR]

This study investigated the cardiac, vasomotor, and myocardial branches of the baroreflex in fibromyalgia using the spontaneous sequence method. Systolic blood pressure (SBP), interbeat interval (IBI), stroke volume (SV), pre‐ejection period (PEP), and total peripheral resistance (TPR) were continuously recorded in 40 fibromyalgia patients and 30 healthy individuals during a cold pressor test and a mental arithmetic task. Sequences of covariation between SBP and IBI (cardiac branch), SV and PEP (myocardial branch), and TPR (vasomotor branch) were identified. Baroreflex sensitivity (BRS) was represented by the slope of the regression line between values in the sequences; baroreflex effectiveness (BEI) was indexed by the proportion of progressive SBP changes that elicited reflex responses. Patients exhibited lower BRS in the three branches, lower BEI in the cardiac and vasomotor branches, and reduced reactivity in cardiac BRS and BEI, SBP, IBI, SV, and PEP. Moreover, BRS and BEI were inversely related to clinical pain, cold pressor pain, depression, trait anxiety, sleep problems, and fatigue. Reduced function of the three baroreflex branches implies diminished resources for autonomic inotropic, chronotropic, and vascular regulation in fibromyalgia. Blunted stress reactivity indicates a limited capacity for autonomic cardiovascular adjustment to situational requirements. The associations of BRS and BEI with pain perception may reflect the antinociceptive effects arising from baroreceptor afferents, where reduced baroreflex function may contribute to the hyperalgesia characterizing fibromyalgia. The associations with affective impairments, sleep problems, and fatigue suggest that baroreflex dysfunctions are also involved in the secondary symptoms of the disorder. Fibromyalgia is associated with autonomic alterations. We analyzed the cardiac, vascular and myocardial branches of the baroreflex in fibromyalgia under rest and stress conditions. Fibromyalgia patients displayed reduced sensitivity and effectiveness of the baroreflex in the three branches. Baroreflex parameters were negatively associated with clinical and evoked pain, depression, anxiety, fatigue and sleep problems in the patients' sample. These results reflect the inhibitory effects arising from the baroreceptors and their contribution to fibromyalgia symptoms. [ABSTRACT FROM AUTHOR]

Observed individual variability in cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV) is extensive, especially during exposure to stressors such as heat. A large part of the observed variation may be related to the reliability (consistency) of the measurement. We therefore examined the test–retest reliability of cBRS and HRV measurements on three separate occasions in 14 young men (age: 24 (SD 5) years), at rest and during whole‐body heating (water‐perfused suit) to raise and clamp oesophageal temperature 0.6°C, 1.2°C and 1.8°C above baseline. Beat‐to‐beat measurements of RR interval and systolic blood pressure (BP) were obtained for deriving HRV (from RR), and cBRS calculated via (i) the spontaneous method, α coefficients and transfer function analysis at each level of heat strain, and (ii) during forced oscillations via squat–stand manoeuvres (0.1 Hz) before and after heating. Absolute values and changes in all cBRS estimates were variable but generally consistent with reductions in parasympathetic activity. cBRS estimates demonstrated poor absolute reliability (coefficient of variation ≥25%), but relative reliability (intraclass correlation coefficient; ICC) of some frequency estimates was acceptable (ICC ≥0.70) during low‐heat strain (ICC: 0.56–0.74). After heating, forced oscillations in BP demonstrated more favourable responses than spontaneous oscillations (better reliability, lower minimum detectable change). Absolute reliability of HRV estimates were poor, but relative reliability estimates were often acceptable (≥0.70). Our findings illustrate how measurement consistency of cardiac autonomic modulation estimates are altered during heat stress, and we demonstrate the possible implications on research design and data interpretation. [ABSTRACT FROM AUTHOR]

Whether part of the blood pressure lowering effects of glyceryl trinitrate (GTN) is the result of centrally mediated reduction in sympathetic activity is debated. In humans, baroreflex activity potentially obscures the central sympatholytic effects of GTN. We examined this in a routine clinical tilt test in a patient with baroreflex failure secondary to previous neck radiotherapy. With reduced baroreflex function we observed an exaggerated fall in blood pressure and reduced sympathetic activity with GTN, supporting a peripheral vasodilation and central sympatholytic effect. [ABSTRACT FROM AUTHOR]

Background: Alcohol abuse is a health concern worldwide. Studies have associated alcohol abuse with cardiovascular impairments. In this study, we investigated differences in the effects of chronic alcohol vapor exposure on cardiovascular function between male and female rats by using the alcohol vapor chamber method to induce alcohol addiction‐like behaviors in rats. Methods: We exposed male and female Long‐Evans rats to alcohol vapor for 14 hours, followed by ethanol withdrawal for 10 hours, for 30 consecutive days or room air (control groups). The animals underwent preparation for the surgical implantation of cannulas into femoral vessels, for allowing the assessment of the basal arterial pressure and heart rate values, baroreflex function, and autonomic activity. Results: Female control rats showed higher basal heart rate compared to male control rats. Chronic alcohol vapor inhalation reduced basal heart rate in females, but not in males; this effect was followed by an increase in the parasympathetic tone of the heart. Further, female rats subjected to alcohol vapor showed an increase in the baroreflex activity. Conclusions: These findings suggest that females are more sensitive to chronic alcohol vapor exposure than males because they had a reduction in basal heart rate and changes in the baroreflex activity. [ABSTRACT FROM AUTHOR]

Mercury is known to cause harmful neural effects affecting the cardiovascular system. Here, we evaluated the chronic effects of low-dose mercury exposure on the autonomic control of the cardiovascular system. Wistar rats were treated for 30 days with HgCl2 (1st dose 4.6 μg/kg followed by 0.07 μg/kg per day, intramuscular) or saline. The femoral artery and vein were then cannulated for evaluation of autonomic control of the hemodynamic function, which was evaluated in awake rats. The following tests were performed: baroreflex sensitivity, Von Bezold-Jarisch reflex, heart rate variability ( HRV) and pharmacological blockade with methylatropine and atenolol to test the autonomic tone of the heart. Exposure to HgCl2 for 30 days slightly increased the mean arterial pressure and heart rate ( HR). There was a significant reduction in the baroreflex gain of animals exposed to HgCl2. Moreover, haemodynamic responses to the activation of the Von Bezold-Jarisch reflex were also reduced. The changes in the spectral analysis of HRV suggested a shift in the sympathovagal balance toward a sympathetic predominance after mercury exposure, which was confirmed by autonomic pharmacological blockade in the HgCl2 group. This group also exhibited reduced intrinsic HR after the double block suggesting that the pacemaker activity of the sinus node was also affected. These findings suggested that the autonomic modulation of the heart was significantly altered by chronic mercury exposure, thus reinforcing that even at low concentrations such exposure might be associated with increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

This study reports on the effects of maternal protein malnutrition on baroreflex ( BR) control of the heart rate and sympathetic nerve activity in the hypertensive male offspring of Wistar rat dams. Wistar rat dams were fed a normal protein ( NP) control (17% protein) or a low protein ( LP; 8% protein) diet during pregnancy and lactation, and their male offspring were studied when 90 days old. In these animals we evaluated spontaneous and induced BR control, the variability of the cardiovascular system and analyzed a direct recording of lumbar sympathetic nervous activity. The 90 day-old LP conscious rats had increased arterial pressure compared to NP, with enhanced low frequency oscillations of the systolic pressure, but no changes in the spontaneous and induced BR control of heart rate. In relation to nerve recordings, we observed similar values in terms of mean, frequency and amplitude between the groups. In addition, we noted that spontaneous and induced BR control of lumbar sympathetic activity in the LP group was similar to the control group. The data indicate that hypertension in the adult rat offspring subjected to perinatal protein malnutrition is not related to baroreflex dysfunction. [ABSTRACT FROM AUTHOR]

Aim Drinking water induces short-term cardiovascular and metabolic changes. These effects are considered to be triggered by gastric distension and osmotic factors, but little is known about the influence of water temperature. Methods We determined, in a randomized crossover study, the acute cardiovascular and metabolic responses to 500 mL of tap water at 3 °C (cold), 22 °C (room) and 37 °C (body) in 12 young humans to ascertain an effect of water temperature. We measured continuous beat-to-beat haemodynamics, skin blood flux with laser-Doppler flowmetry and resting energy expenditure by indirect calorimetry starting with a 30-min baseline followed by a 4-min drink period and a subsequent 90-min post-drink observation. Results Ingestion of cold- and room-tempered water led to decreased heart rate ( P < 0.01) and double product ( P < 0.01), and increased stroke volume ( P < 0.05); these effects were not observed with body-tempered water. Drinking cold- and room-, but not body-tempered water, led to increased high frequency power of heart rate variability ( P < 0.05) and baroreflex sensitivity ( P < 0.05). Cold- and room-tempered water increased energy expenditure over 90 min by 2.9% ( P < 0.05) and 2.3% (ns), respectively, accompanied by a diminished skin blood flux ( P < 0.01), thereby suggesting that both small increases in heat production together with decreased heat loss contribute to warming up the ingested water to intra-abdominal temperature levels. Conclusions Overall, ingestion of cold- and room-, but not body-tempered water reduced the workload to the heart through a reduction in heart rate and double product which could be mediated by an augmented cardiac vagal tone. [ABSTRACT FROM AUTHOR]

The baroreflex consists of a negative feedback loop adjusting heart activity to blood pressure fluctuations. This review is concerned with interactions between baroreflex function and behavior. In addition to changes in baroreflex cardiac control subject to behavioral manipulations, interindividual differences in reflex function predicted psychological and central nervous features. The sensitivity of the reflex was inversely related to cognitive performance, evoked potential amplitudes, experimental pain sensitivity, and the severity of clinical pain. Possible variables moderating the strength of the associations are tonic blood pressure, gender, and psychiatric disease. It is suggested that these observations reflect inhibition of higher brain function by baroreceptor afferents. While in many cases increased baroreflex function implies stronger inhibition, individual and situational factors modulate the behavioral impact of cardiac regulation. [ABSTRACT FROM AUTHOR]

Altered autonomic control of the cardiovascular system in chronic kidney disease ( CKD) contributes to an increased risk of cardiovascular events. The aim of the present study was to determine whether and when autonomic dysfunction occurs in a conscious, telemetered, rodent model of CKD., In Lewis polycystic kidney ( LPK; n = 8) and Lewis ( n = 8) rats, blood pressure ( BP), heart rate ( HR), HR variability ( HRV), systolic BP variability ( SBPV) and baroreflex sensitivity ( BRS) were determined from 10 to 16 weeks of age., The LPK rats had higher systolic BP (average across all ages: 230 ± 10 vs 122.6 ± 0.3 mm Hg; P < 0.001), increased SBPV (average across all ages: 13.9 ± 1.9 vs 5.2 ± 0.2 mm Hg2; P < 0.01) and reduced low-frequency HRV power (average across all ages: 1.5 ± 0.3 vs 2.6 ± 0.2 msec2; P < 0.05). Between 10 and 12 weeks of age, SBPV increased twofold in the LPK rat (8.13 ± 1.05 vs 16.10 ± 1.31 mmHg2 for 10 vs 12 weeks of age, respectively; P < 0.001), coinciding with an approximate 40% reduction in BRS (1.32 ± 0.14 vs 0.79 ± 0.11 ms/mmHg for 10 vs 12 weeks of age, respectively; P < 0.05). There was no difference in BRS between LPK and Lewis rats at 10 weeks of age; however, from 12 weeks onwards, BRS was reduced in LPK rats (0.75 ± 0.01 vs 1.17 ± 0.04 ms/mmHg; P < 0.01)., Baroreceptor regulation of HR becomes impaired between 10 and 12 weeks of age in the LPK rat, coinciding with an increase in SBPV. Preventing baroreflex dysfunction in CKD may reduce SBPV and the associated mortality risks. [ABSTRACT FROM AUTHOR]

This article evaluates the suitability of low frequency ( LF) heart rate variability ( HRV) as an index of sympathetic cardiac control and the LF/high frequency ( HF) ratio as an index of autonomic balance. It includes a comprehensive literature review and a reanalysis of some previous studies on autonomic cardiovascular regulation. The following sources of evidence are addressed: effects of manipulations affecting sympathetic and vagal activity on HRV, predictions of group differences in cardiac autonomic regulation from HRV, relationships between HRV and other cardiac parameters, and the theoretical and mathematical bases of the concept of autonomic balance. Available data challenge the interpretation of the LF and LF/ HF ratio as indices of sympathetic cardiac control and autonomic balance, respectively, and suggest that the HRV power spectrum, including its LF component, is mainly determined by the parasympathetic system. [ABSTRACT FROM AUTHOR]

Paced 0.1 Hz breathing causes high-amplitude HR oscillation, triggering resonance in the cardiovascular system (CVS). This oscillation is considered to be a primary therapeutic factor in HRV biofeedback treatments. This study examined whether rhythmical skeletal muscle tension (RSMT) can also cause 0.1 Hz resonance in the CVS, and compared oscillatory reactivity in CVS functions caused by RSMT and paced breathing (PB). Sixteen young healthy participants completed five tasks: baseline, three RSMT tasks at frequencies of 0.05, 0.1, and 0.2 Hz, and a 0.1 Hz PB task. ECG, respiration, finger pulse, and skin conductance data were collected. Results showed that 0.1 Hz RSMT as well as 0.1 Hz PB triggered resonance in the CVS and caused equivalent oscillations in all measured CVS functions, although in women, RSMT compared to PB caused lower HR oscillation. Clinical application of 0.1 Hz RSMT is discussed. [ABSTRACT FROM AUTHOR]

1. Impairmant of baroreflex sensitivity (BRS) has been implicated in the reduction of heart rate variability (HRV) and in the increased risk of death after myocardial infarction (MI). In the present study, we investigated whether the additional impairment in BRS induced by sinoaortic baroreceptor denervation (SAD) in MI rats is associated with changes in the low-frequency (LF) component of HRV and increased mortality rate. 2. Rats were randomly divided into four groups: control, MI, denervated (SAD) and SAD + MI rats. Left ventricular (LV) function was evaluated by echocardiography. Autonomic components were assessed by power spectral analysis and BRS. 3. Myocardial infarction (90 days) reduced ejection fraction (by ∼42%) in both the MI and SAD + MI groups; however, an increase in LV mass and diastolic dysfunction were observed only in the SAD + MI group. Furthermore, BRS, HRV and the LF power of HRV were reduced after MI, with an exacerbated reduction seen in SAD + MI rats. The LF component of blood pressure variability (BPV) was increased in the MI, SAD and SAD + MI groups compared with the control group. Mortality was higher in the MI groups compared with the non-infarcted groups, with an additional increase in mortality in the SAD + MI group compared with the MI group. Correlations were obtained between BRS and the LF component of HRV and between LV mass and the LF component of BPV. 4. Together, the results indicate that the abolishment of BRS induced by SAD in MI rats further reduces the LF band of HRV, resulting in a worse cardiac remodelling and increased mortality in these rats. These data highlight the importance of this mechanism in the prognosis of patients after an ischaemic event. [ABSTRACT FROM AUTHOR]

Fibromyalgia (FM) is characterized by generalized muscle pain, low muscle strength and autonomic dysfunction. Heart rate (HR) variability (HRV) is reduced in individuals with FM increasing their risk for cardiovascular morbidity and mortality. We tested the hypothesis that resistance exercise training (RET) improves HRV, baroreflex sensitivity (BRS) and muscle strength in women with FM. Women with FM ( n = 10) and healthy controls ( n = 9), aged 27–60 years, were compared at baseline. Only women with FM underwent supervised RET 2 days per week for 16 weeks. Baseline and post-training measurements included HRV and spontaneous baroreflex sensitivity (BRS, alpha index) from continuous electrocardiogram and blood pressure (BP) recorded with finger plethysmography during 5 min in the supine position. RR interval, total power, log transformed (Ln) squared root of the standard deviation of RR interval (RMSSD), low-frequency power and BRS were lower ( P<0·05), and HR and pulse pressure were higher ( P<0·05) in women with FM than in healthy controls. After RET, mean (SEM) total power increased (387 ± 170 ms2, P<0·05), RMSSD increased (0·18 ± 0·08 Ln ms, P<0·05) and Ln of high-frequency power increased (0·54 ± 0·27 Ln ms2, P = 0·08) in women with FM. Upper and lower body muscle strength increased by 63% and 49% ( P<0·001), and pain perception decreased by 39% in women with FM. There were no changes in BRS, HR and BP after RET. Our study demonstrates that RET improves total power, cardiac parasympathetic tone, pain perception and muscle strength in women with FM who had autonomic dysfunction before the exercise programme. [ABSTRACT FROM AUTHOR]

Aim: Astronauts commonly return from space with altered short-term cardiovascular dynamics and blunted baroreflex sensitivity. Although many studies have addressed this issue, post-flight effects on the dynamic circulatory control remain incompletely understood. It is not clear how long the cardiovascular system needs to recover from spaceflight as most post-flight investigations only extended between a few days and 2 weeks. Methods: In this study, we examined the effect of short-duration spaceflight (1–2 weeks) on respiratory-mediated cardiovascular rhythms in five cosmonauts. Two paced-breathing protocols at 6 and 12 breaths min−1 were performed in the standing and supine positions before spaceflight, and after 1 and 25 days upon return. Dynamic baroreflex function was evaluated by transfer function analysis between systolic pressure and the RR intervals. Results: Post-flight orthostatic blood pressure control was preserved in all cosmonauts. In the standing position after spaceflight there was an increase in heart rate (HR) of approx. 20 beats min−1 or more. Averaged for all five cosmonauts, respiratory sinus dysrhythmia and transfer gain reduced to 40% the day after landing, and had returned to pre-flight levels after 25 days. Low-frequency gain decreased from 6.6 (3.4) [mean (SD)] pre-flight to 3.9 (1.6) post-flight and returned to 5.7 (1.3) ms mmHg−1 after 25 days upon return to Earth. Unlike alterations in the modulation of HR, blood pressure dynamics were not significantly different between pre- and post-flight sessions. Conclusion: Our results indicate that short-duration spaceflight reduces respiratory modulation of HR and decreases cardiac baroreflex gain without affecting post-flight arterial blood pressure dynamics. Altered respiratory modulation of human autonomic rhythms does not persist until 25 days upon return to Earth. [ABSTRACT FROM AUTHOR]

The static relationship between heart rate (HR) and the activity of either vagal or sympathetic nerves is roughly linear within the physiological range of HR variations. The dynamic control of HR by autonomic nerves is characterized by a fixed time delay between the onset of changes in nerve activity and the onset of changes in HR. This delay is much longer for sympathetically than for vagally mediated changes in HR. In addition, the kinetics of the HR responses shows the properties of a low-pass filter with short (vagal) and long (sympathetic) time constants. These differences might be secondary to differences in nervous conduction times, width of synaptic cleft, kinetics of receptor activation and post-receptor events. Because of the accentuated low-pass filter characteristics of the HR response to sympathetic modulation, sympathetic influences are almost restricted to the very-low-frequency component of HR variability, but the chronotropic effects of vagal stimulation usually predominate over those of sympathetic stimulation in this frequency band. Oscillations in cardiac sympathetic nerve activity are not involved in respiratory sinus arrhythmia (high-frequency component) and make a minor contribution to HR oscillations of approximately 10-s period (low-frequency component of approximately 0.1 Hz), at least in the supine position. In the latter case, HR oscillations are derived mainly from a baroreflex, vagally mediated response to blood pressure Mayer waves. Beta-blockers and centrally acting sympathoinhibitory drugs share the ability to improve the baroreflex control of HR, possibly through vagal facilitation, which might be beneficial in several cardiovascular diseases. [ABSTRACT FROM AUTHOR]

1. Blood pressure and organ perfusion are controlled by a variety of cardiovascular control systems, such as the baroreceptor reflex and the renin–angiotensin system (RAS), and by local vascular mechanisms, such as shear stress-induced release of nitric oxide (NO) from the endothelium and the myogenic vascular response. Deviations in arterial blood pressure from its set point activate these mechanisms in an attempt to restore blood pressure and/or secure organ perfusion. However, the response times at which different cardiovascular mechanisms operate differ considerably (e.g. blood pressure control by the RAS is slower than blood pressure control via the baroreceptor reflex). 2. Owing to these different response times, some cardiovascular control systems affect blood pressure more rapidly and others more slowly. Thus, identifying the frequency components of blood pressure variability (BPV) by power spectral analysis can potentially provide important information on individual blood pressure control mechanisms. 3. Evidence is presented that the RAS, catecholamines, endothelial-derived NO and myogenic vascular function affect BPV at very low frequencies (0.02–0.2 Hz) and that low-frequency (LF) BPV (0.2–0.6 Hz) is affected by sympathetic modulation of vascular tone and endothelial-derived NO in rats. In humans, LF BPV (0.075–0.15 Hz) is affected by sympathetic modulation of vascular tone and myogenic vascular function. The impact of the RAS and endothelial-derived NO on BPV in humans requires further investigation. 4. In conclusion, power spectral analysis is a powerful diagnostic tool that allows identification of pathophysiological mechanisms contributing to cardiovascular diseases, such as hypertension, heart failure and stroke, because it can separate slow from fast cardiovascular control mechanisms. The limitation that some cardiovascular control mechanisms affect the same frequency components of BPV requires the combination of blood pressure spectral analysis with other techniques. [ABSTRACT FROM AUTHOR]

1. The present study assesses the effects of autonomic blockade (α- and β-adrenoceptor and cholinergic) on cardiovascular function studied by heart rate variability (HRV), blood pressure variability (BPV) and baroreflex sensitivity in rats using non-linear dynamics. Little is known about the influence of pharmacological autonomic nervous system interventions on non-linear cardiovascular regulatory indices. 2. In 13 conscious rats, heart rate and aortic blood pressure were measured continuously before, during and after autonomic blockade with atropine, phentolamine and propranolol. Non-linear scaling properties were studied using 1/f slope, fractal dimension and long- and short-term correlation. Non-linear complexity was described with correlation dimension, Lyapunov exponent and approximate entropy. Non-linear indices were compared with linear time and frequency domain indices. 3. β-Adrenoceptor blockade did not alter the non-linear characteristics of HRV and BPV, although low-frequency power of HRV was depressed. α-Adrenoceptor blockade decreased the scaling behaviour of HRV, whereas cholinergic blockade decreased the complexity of the non-linear system of HRV. For BPV, the scaling behaviour was increased during α-adrenoceptor blockade and the complexity was increased during cholinergic blockade. The linear indices of HRV and BPV were decreased. 4. The present results indicate that the β-adrenoceptor system has little involvement in the generation of non-linear HRV and BPV in rats. 5. α-Adrenoceptor blockade mostly influenced the scaling properties of the time series, whereas cholinergic blockade induced changes in the complexity measures. 6. The absence of the baroreflex mechanism can trigger a compensatory feed-forward system increasing the complexity of BPV. [ABSTRACT FROM AUTHOR]

Heart Rate Variability and Baroreflex-Related Vagal Activity. Introduction: Many previous studies have suggested that the high-frequency (HF) power of the heart rate variability may represent cardiac vagal activity although direct evidence of a correlation between the HF and vagal neuronal activity is still lacking. In the present study, we performed a regression analysis of the HF and vagal neurograms. Methods and Results: Experiments were carried out on adult male Sprague-Dawley rats anesthetized with a continuous infusion of pentobarbital sodium. The baroreflex-related vagus neuronal activities were obtained by nerve or single-fiber recordings. The transient baroreflex response was employed to alter vagus neuronal activities using a bolus injection of phenylephrine (PE). On-line power spectral analysis of the heart rate and a vagal neurogram was performed during the acute baroreflex response. During the test period, systemic arterial pressure immediately increased in response to the PE injection, after which the R–R interval (RR), HF (0.6–2.4 Hz), and vagus nerve and unit activities all dramatically increased. Both nerve and unit activities exhibited good correlations (r ≥ 0.7 in all nerve recordings and r ≥ 0.6 in 91% of single-fiber recordings) with the HF. There were insignificant differences between the right- and left-side baroreflex-related vagus nerve recordings. Conclusion: Our present study provides a direct linkage between the HF and vagus neuronal electrical activity in anesthetized rats. (J Cardiovasc Electrophysiol, Vol. 16, pp. 1-6, August 2005) [ABSTRACT FROM AUTHOR]

Impaired Baroreflex Gain and Inappropriate Sinus Tachycardia. Introduction:The aim of this study was to determine the characteristics of heart rate variability (HRV), blood pressure variability (BPV), and baroreflex gain (BRG) at rest and during orthostatic stress in patients with clinical criteria of inappropriate sinus tachycardia (IST).Methods and Results:Beat-to-beat HRV and BPV, measured by time- and frequency-domain methods, and noninvasive BRG, calculated by cross-spectral analysis, were obtained during 10 minutes both at rest and during the stabilization phase (5–15 min) of orthostatic stress at 60° in 8 patients with clinical criteria of IST and 9 healthy volunteers (CON). IST patients had a higher resting mean heart rate (78.8± 5.3 vs 58.5± 4.2 beats/min, P= 0.01) and mean blood pressure (90.4± 2.4 vs 72.0± 4.2 mmHg; P= 0.002). RMSSD, pNN50m, and BRG were significantly reduced in IST patients at rest. BRG during orthostatic stress (7.2± 0.8 vs 20.3 (2.4 ms/mmHg, P<0.01) was significantly reduced in IST patients.Δ BRG (−16.9%± 11 vs−50.1%± 5, P= 0.02) was markedly blunted during orthostatic stress in IST patients.Conclusion:BRG was markedly impaired both at rest and during orthostatic stress in IST patients. This alteration may be responsible for the higher resting heart rate and mean blood pressures seen at rest and may facilitate tachycardia during orthostatic stress. A primary alteration in sinus node automaticity coupled with impaired BRG determines heart rate response to orthostatic stress in patients with IST.(J Cardiovasc Electrophysiol, Vol. 16, pp. 64-68, January 2005) [ABSTRACT FROM AUTHOR]

Background: Congestive cardiac failure is associated with increased sympathetic activity and impaired baroreflex function. We sought to test the hypothesis that these patients also have blunted response of beat-to-beat QT interval variability during orthostatic challenge.Methods: We compared beat-to-beat heart rate and QT interval data in 17 patients with congestive cardiac failure and 17 age-matched normal controls in supine normal breathing, supine controlled breathing, and standing controlled breathing conditions. The ECG data were acquired in lead II configuration at a sampling rate of 1000 Hz.Results: Supine controlled breathing was associated with an increase in spectral HF power (0.15–0.5 Hz) of HR and QT interval time series compared to spontaneous breathing condition only in controls. While there were significant changes in HR, HR LF power, HR LF/HF ratios, and QT variability measures in standing posture in controls, there were no such changes in patients.Conclusions: This impairment of postural changes of HR variability is most likely due to an impaired baroreceptor function in patients with congestive heart failure. The etiology of this is likely due to an increased cardiac sympathetic and a decreased vagal function. However, the relationship of postural changes in beat-to-beat QT interval variability and baroreflex need further investigation.A.N.E. 2004;9(4):323–329 [ABSTRACT FROM AUTHOR]

Abstract Background In diabetic patients, impairment of the cardiovagal limb of the baroreflex has been well established. However, the role of sympathetic mediated baroreflex vasomotor control of the blood vessels is not well defined. We therefore assessed the vasomotor responses to sinusoidal baroreceptor stimulation in diabetic patients. Materials and methods We studied 14 type II diabetic patients (age; 57 ± 7 years) and 18 healthy controls (age; 59 ± 11 years). Oscillatory neck suction was applied at 0·1 Hz to assess the sympathetic modulation of the heart and blood vessels, and at 0·2 Hz to assess the effect of parasympathetic stimulation on the heart. Breathing was paced at 0·25 Hz. Spectral analysis was used to evaluate the oscillatory responses of RR-interval and blood pressure. Results The diabetic patients showed a significantly lower RR-interval response (P < 0·05) to the 0·1 Hz neck suction (2·52 ± 0·50–3·62 ± 0·54 ln ms2 ) than the controls (4·23 ± 0·31–6·74 ± 0·36 ln ms2 ). The increase in power of 0·1 Hz systolic blood pressure oscillations during 0·1 Hz suction was also significantly smaller (P < 0·05) in the diabetics (1·17 ± 0·44–1·69 ± 0·44 mmHg2 ) than in the controls (1·60 ± 0·29 mmHg2 -5·87 ± 1·25 mmHg2 ). The magnitude of the peak of the 0·2 Hz oscillation in the RR-interval in response to 0·2 Hz neck stimulation was significantly greater (P < 0·05) in the controls (3·42 ± 0·46 ln ms2 ) than in the diabetics (1·58 ± 0·44 ln ms2 ). Conclusion In addition to cardiovagal dysfunction, baroreflex-mediated sympathetic modulation of the blood vessels is impaired in type II diabetic patients. [ABSTRACT FROM AUTHOR]

'Department of Physiology and Functional Genomics, University of Florida. U.S.A. This review focuses on the dysfunction of the intrinsic brain renin—angiotensin system (RAS) in the pathogenesis of hypertension. Hyperactivity of the brain RAS plays a critical role in mediating hypertension in both humans and animal models of hypertension, including the spontaneously hypertensive rat (SHR). The specific mechanisms by which increased brain RAS activity results in hypertension arc not well understood but include increases in sympathetic vasomotor tone and impaired arterial baroreflex function. We discuss the contribution of endogenous angiotensin (Ang) 11 actions on presympathetic vasomotor rostral ventrolateral medulla neurons to enhance sympathetic activity and maintain hypertension. In addition, we discuss Ang II-induced attenuation of afferent baroreceptor feedback within the nucleus tractus solitarius and its relevance to the development of hypertension. We also outline the cellular and molecular mechanisms of Ang II signal transduction that may be critical for the initiation and establishment of hypertension. In particular, we present evidence for a phosphoinositidc-3-kinase-depcndent signaling pathway that appears to contribute to hypertension in the SHR, possibly via augmented Ang 11-induced increases in neuronal firing rate and enhanced transcriptional noradrenaline neuromodulation. Finally, we outline future directions in utilizing our understanding of the brain RAS dysfunction in hypertension for the development of improved therapeutic intervention in hypertension. [ABSTRACT FROM AUTHOR]

Abstract Background Healthy ageing has several effects on the autonomic control of the circulation. Several studies have shown that baroreflex-mediated vagal control of the heart deteriorates with age, but so far there is little information regarding the effect of ageing on sympathetically mediated baroreflex responses. The aim of this study was to assess the effects of ageing on baroreflex control of the heart and blood vessels. Materials and Methods In 40 healthy volunteers, aged 20–87 years, we applied oscillatory neck suction at 0·1 Hz to assess the sympathetic modulation of the heart and blood vessels and at 0·2 Hz to assess the effect of parasympathetic stimulation on the heart. Breathing was maintained at 0·25 Hz. Blood pressure, electrocardiographic RR intervals and respiration were recorded continuously. Spectral analysis was used to evaluate the magnitude of the low-frequency (0·03–0·14 Hz) and high-frequency (0·15–0·50 Hz) oscillations in the RR interval and blood pressure. Responses to neck suction were assessed as the change in power of the RR interval and blood pressure fluctuations at the stimulation frequency from baseline values. Results Resting low- and high-frequency powers of the RR interval decreased significantly with age (P < 0·01). However, the low-frequency power of systolic blood pressure did not correlate with age. Spontaneous baroreflex sensitivity (alpha-index) showed a significant inverse correlation with age (r = -0·46, P < 0·05). Responses of the RR interval and systolic blood pressure to 0·1 Hz neck suction stimulation were not related to age, however, the RR interval response to 0·2 Hz neck suction declined significantly with age (r = -0·61, P < 0·01). Conclusions These results confirm an age-related decrease in cardiovagal baroreflex responses. However, sympathetically mediated baroreflex control of the blood vessels is preserved with age. [ABSTRACT FROM AUTHOR]

Background: We assessed the behavior of the baroreflex (BR) gain in chronic heart failure (CHF) patients using the spectral analysis method during application of a forcing stimulus, i.e. respiration.Methods: Simultaneous RR interval and arterial pressure fluctuation recordings were obtained during two random-order periods of voluntary paced-breathing (0.15 Hz and 0.25 Hz) in seven patients with moderate CHF (NYHA class II/III; EF, 30+/-9%; peak VO(2), 18+/-5 ml kg(-1) min(-1)) and six age-matched controls. BR gain was assessed in the time (sequential method) and frequency (cross-spectral gain in the low and high frequency) domains.Results: Slower breathing was associated with a BR gain decrease in CHF patients whereas a BR gain increase was evidenced in controls (BR gain: 6+/-5 ms mmHg(-1) at 0.25 Hz vs. 4+/-3 ms mmHg(-1) at 0.15 Hz, P<0.05 in CHF; BR gain: 12+/-7 ms mmHg(-1) at 0.25 Hz vs. 15+/-7 ms mmHg(-1) at 0.15 Hz, P<0.05 in controls).Conclusions: Voluntary breathing, which involves cortical centers in the brain, had major effects on cardiovascular system controller gain in CHF patients, indicating an impairment of the central neural regulation of the autonomic outflow. [ABSTRACT FROM AUTHOR]