Rate Reflex Sensitivity Research Articles

Transcutaneous auricular vagus nerve stimulation augments postprandial inhibition of ghrelin.

Vagus nerve stimulation (VNS) facilitates weight loss in animals and patients treated with VNS for depression or epilepsy. Likewise, chronic transcutaneous auricular VNS (taVNS) reduces weight gain and improves glucose tolerance in Zucker diabetic fatty rats. If these metabolic effects of taVNS observed in rats translate to humans is unknown. Therefore, the hypothesis of this study was that acute application of taVNS affects glucotropic and orexigenic hormones which could potentially facilitate weight loss and improve glucose tolerance if taVNS were applied chronically. In two single‐blinded randomized cross‐over protocols, blood glucose levels, plasma concentrations of insulin, C‐peptide, glucagon, leptin, and ghrelin, together with heart rate variability and baroreceptor‐heart rate reflex sensitivity were determined before and after taVNS (left ear, 10 Hz, 300 µs, 2.0–2.5 mA, 30 min) or sham‐taVNS (electrode attached to ear with the stimulator turned off). In a first protocol, subjects (n = 16) were fasted throughout the protocol and in a second protocol, subjects (n = 10) received a high‐calorie beverage (220 kCal) after the first blood sample, just before initiation of taVNS or sham‐taVNS. No significant effects of taVNS on heart rate variability and baroreceptor‐heart rate reflex sensitivity and only minor effects on glucotropic hormones were observed. However, in the second protocol taVNS significantly lowered postprandial plasma ghrelin levels (taVNS: −115.5 ± 28.3 pg/ml vs. sham‐taVNS: −51.2 ± 30.6 pg/ml, p < 0.05). This finding provides a rationale for follow‐up studies testing the hypothesis that chronic application of taVNS may reduce food intake through inhibition of ghrelin and, therefore, may indirectly improve glucose tolerance through weight loss.

Activation of the cholinergic antiinflammatory reflex by occipitoatlantal decompression and transcutaneous auricular vagus nerve stimulation.

The parasympathetic-mediated inflammatory reflex inhibits excessive proinflammatory cytokine production. Noninvasive techniques, including occipitoatlantal decompression (OA-D) and transcutaneous auricular vagus nerve stimulation (taVNS), have been demonstrated to increase parasympathetic tone. To test the hypothesis that OA-D and taVNS increase parasympathetic nervous system activity and inhibit proinflammatory cytokine mobilization and/or production. Healthy adult participants were randomized to receive OA-D (5min of OA-D followed by 10min of rest; n=8), taVNS (15min; n=9), or no intervention (15min, time control; n=10) on three consecutive days. Before and after these interventions, saliva samples were collected for determination of the cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF-α). Arterial blood pressure and the electrocardiogram were recorded for a 30-min baseline, throughout the intervention, and during a 30-min recovery period to derive heart rate and blood pressure variability markers as indices of vagal and sympathetic control. OA-D and taVNS increased root mean square of successive RR interval differences (RMSSD) and high frequency heart rate variability, which are established markers for parasympathetic modulation of cardiac function. In all three groups, the experimental protocol was associated with a significant increase in salivary cytokine concentrations. However, the increase in IL-1β was significantly less in the taVNS group (+66±13pg/mL; p<0.05) than in the time control group (+142±24pg/mL). A similar trend was observed in the taVNS group for TNF-α (+1.7±0.3pg/mL vs. 4.1±1.3pg/mL; p<0.10). In the OA-D group baseline IL-6, IL-8, and TNF-α levels on the third study day were significantly lower than on the first study day (IL-6: 2.3±0.4 vs. 3.2±0.6pg/mL, p<0.05; IL-8: 190±61 vs. 483±125pg/mL, p <0.05; TNF-α: 1.2±0.3 vs. 2.3±0.4pg/mL, p<0.05). OA-D decreased mean blood pressure from the first (100±8mmHg) to the second (92±6mmHg; p<0.05) and third (93±8mmHg; p<0.05) study days and reduced low frequency spectral power of systolic blood pressure variability (19±3mmHg2 after OA-D vs. 28±5mmHg2 before OA-D; p<0.05), a marker of sympathetic modulation of vascular tone. OA-D also increased baroreceptor-heart rate reflex sensitivity from the first (13.7±3.0ms/mmHg) to the second (18.4±4.3ms/mmHg; p<0.05) and third (16.9±4.2ms/mmHg; p<0.05) study days. Both OA-D and taVNS elicited antiinflammatory responses that were associated with increases in heart rate variability-derived markers for parasympathetic function. These findings suggest that OA-D and taVNS activate the parasympathetic antiinflammatory reflex. Furthermore, an antihypertensive effect was observed with OA-D that may be mediated by reduced sympathetic modulation of vascular tone and/or increased baroreceptor reflex sensitivity.

Finger volume pulse waveforms facilitate reliable assessment of heart rate variability, but not blood pressure variability or baroreflex function.

BackgroundWe sought to determine whether heart rate variability (HRV), blood pressure (BP) variability, and baroreceptor-heart rate reflex sensitivity can be reliably assessed using finger volume pulse waveforms obtained from the commercially available EndoPAT device.MethodsNon-invasive BP (Finometer Pro as a non-invasive standard) and finger volume (EndoPAT) waveforms were recorded in 65 adults (37 ± 14 years; 60% female) and systolic BP and heart rate (HR) time series were derived after calibrating the EndoPAT signal based on systolic and diastolic BP values obtained by a sphygomomanometer. Transfer function analyses were performed to test for coherence between systolic BP and HR time series derived from the Finometer and EndoPAT devices. Time-domain HRV parameters, frequency domain HR and systolic BP variability parameters, and baroreflex sensitivity (sequence technique) were computed from Finometer- and EndoPAT-derived time series and intraclass correlation coefficients (ICC) were calculated.ResultsSquared coherence between systolic BP time series derived from the Finometer and EndoPAT devices was low, suggesting poor correlation. In contrast, squared coherence between HR time series derived from the two devices was excellent [High Frequency (HF) = 0.80, Low Frequency (LF) = 0.81], with gain values close to 1.0. ICC values for time- and frequency-domain HRV parameters were excellent (>0.9 except for relative HF HRV, which was 0.77), while ICC values for frequency-domain BP variability parameters and baroreceptor-HR reflex sensitivity were low.ConclusionsFinger volume pulse waveforms can be used to reliably assess both time-domain and frequency-domain HR variability. However, frequency domain BP variability parameters cannot be reliably assessed from finger volume pulse waveforms using the simple calibration technique used in this study.

Commentaries on Viewpoint: Is the resting bradycardia in athletes the result of remodeling of the sinoatrial node rather than high vagal tone?

Commentaries on Viewpoint: Is the resting bradycardia in athletes the result of remodeling of the sinoatrial node rather than high vagal tone?

Prognostic Implications of Baroreflex Sensitivity in Heart Failure Patients in the Beta-Blocking Era

This study investigated the clinical correlates and prognostic value of depressed baroreceptor-heart rate reflex sensitivity (BRS) among patients with heart failure (HF), with and without beta-blockade. Abnormalities in autonomic reflexes play an important role in the development and progression of HF. Few studies have assessed the effects of beta-blockers on BRS in HF. The study population consisted of 103 stable HF patients, age (median [interquartile range]) 54 years (48 to 57 years), with New York Heart Association (NYHA) functional class > or =III in 22, and with a left ventricular ejection fraction (LVEF) of 30% (24% to 36%), treated with beta-blockers; and 144 untreated patients, age 55 years (48 to 60 years), with NYHA functional class > or =III in 47%, and an LVEF of 26% (21% to 30%). They underwent BRS testing (phenylephrine technique). In both treated and untreated patients, a lower BRS was associated with a higher (> or =III) NYHA functional class (p = 0.0002 and p < 0.0001, respectively); a more severe (> or =2) mitral regurgitation (p = 0.007 and p = 0.0002), respectively; a lower LVEF (p = 0.0004 and p = 0.001, respectively), baseline RR interval (p = 0.0004 and p = 0.0002, respectively), and SDNN (p < 0.0001, p = 0.002, respectively); and a higher blood urea nitrogen (p = 0.004, p < 0.0001, respectively). Clinical variables explained only 43% of BRS variability among treated and 36% among untreated patients. During a median follow-up of 29 months, 17 of 103 patients and 55 of 144 patients, respectively, experienced a cardiac event. A depressed BRS (<3.0 ms/mm Hg) was significantly associated with the outcome, independently of known risk predictors and beta-blocker treatment (adjusted hazard ratio: 3.0 [95% confidence interval: 1.5 to 5.9], p = 0.001). Baroreceptor-heart rate reflex sensitivity does not simply mirror the pathophysiological substrate of HF. A depressed BRS conveys independent prognostic information that is not affected by the modification of autonomic dysfunction brought about by beta-blockade.

Exercise Training Fails to Modify Arterial Baroreflex Sensitivity in Ovariectomized Female Rats

In men, exercise training attenuates age-related reduction in baroreflex sensitivity, which is related to cardiovascular health. It is unknown, however, if this holds true for post-menopausal women. We examined the effects of exercise training on baroreceptor-heart rate (HR) reflex sensitivity in ovariectomized (OVX) and sham-operated (SO) Wistar-Kyoto rats. At the age of 8 weeks, OVX and SO rats were assigned to either sedentary or exercise-trained group. Exercise training was performed on a treadmill 5 days per week. At the age of 20 weeks, baroreflex sensitivity in response to increases in blood pressure (BRSinc) and decreases in blood pressure (BRSdec) were evaluated by injections of phenylephrine and sodium nitroprusside, respectively. Both BRSinc and BRSdec were significantly reduced in sedentary OVX rats compared with sedentary SO rats. Exercise training decreased resting HR and BRSdec, but had no effect on BRSinc in SO rats. In OVX rats, exercise training decreased resting HR but modified neither BRSdec nor BRSinc. We conclude that withdrawal of female sex hormones in normotensive female rats is associated with reduced baroreflex sensitivity in response to both increase and decrease in blood pressure and that exercise training fails to modulate the decline of BRSinc associated with withdrawal of female sex hormones. To maintain high level of BRSinc in post-menopausal women, hormone replacement therapy may be needed.

Comparison of the Effects of VVI Versus DDD Pacing on Cardiac Baroreflex Function

Conventional baroreceptor-heart rate (HR) reflex sensitivity cannot be examined in chronotropically incompetent patients or in pacemaker recipients. However, cardiac baroreceptor reflex sensitivity (BRS)-stroke volume (SV), which is closely and linearly correlated with BRS-HR, may be an alternative in that population. The aim of this study was to compare the BRS-SV in pacemaker recipients with a fixed HR paced in VVI versus DDD modes in the supine and upright positions. The pacing mode was set randomly to DDD or VVI with complete atrial and/or ventricular capture, then crossed over to the alternate mode in 9 recipients of dual-chamber pacemakers with atrioventricular (AV) block. Beat-to-beat mean blood pressure and SV were measured in the supine and upright positions, using a tilt table. The BRS-SV, expressed in %/mmHg, was the ratio of low-frequency (LF) power to total power (TP) of SV variability, measured by spectral analysis of spontaneous variations in mean blood pressure and SV. BRS-SV was significantly lower in the VVI than in the DDD mode in the supine (37.2 +/- 26.7 vs 14.5 +/- 7.7%/mmHg) and upright (22.9 +/- 16.9 vs 10.6 +/- 6.6%/mmHg) positions (P < 0.05 for both comparisons). VVI pacing is adverse from the standpoint of cardiac autonomic baroreflex function. A decreased BRS-SV may be one of the factors involved in the hemodynamic intolerance associated with VVI pacing.

Determination of Baroreceptor‐Stroke Volume Reflex Sensitivity by Power Spectral Analysis: A Quantitative Probe of Baroreceptor‐Cardiac Reflex

Baroreceptor‐cardiac reflex, which consists of baroreceptor‐induced chronotropic and inotropic actions, is a very useful index of cardiac sympathovagal balance. Baroreceptor‐heart rate reflex sensitivity, which reflects baroreceptor‐induced chronotropic action, has been used as a marker of baroreceptor‐cardiac reflex. However, it cannot be used in patients with chronotropic incompetence and/or implanted cardiac pacemaker. We hypothesized that baroreceptor‐stroke volume (SV) reflex sensitivity, which reflects baroreceptor‐induced inotropic action, may also be a useful method for measurement of baroreceptor‐cardiac reflex, similar to the baroreceptor‐heart rate reflex sensitivity. To test this hypothesis, we measured baroreceptor‐SV reflex sensitivity expressed as ratio of low frequency (LF) power to total power of SV fluctuation (LF/TPsv: %/mmHg) by spectral analysis of mean blood pressure and SV fluctuations, the gain in low‐frequency band between two signals in supine and 60° upright positions, and compared these values to baroreceptor‐heart rate reflex sensitivity in 14 healthy subjects. Baroreceptor‐SV reflex sensitivity correlated significantly with baroreceptor‐heart rate reflex sensitivity (r = 0.73, p < 0.0001). In addition, baroreceptor‐SV reflex sensitivity correlated significantly and positively with high frequency (HF) power (r = 0.57, p < 0.005) and negatively with LF/HF ratio (r = − 0.57, p < 0.005) in power spectral analysis of R‐R interval variability. Moreover, baroreceptor‐SV reflex sensitivity in LF/TPSV correlated positively with the R‐R interval (r = 0.70, p < 0.0001) and negatively with diastolic blood pressure (r = − 0.50, p < 0.01). We conclude that baroreceptor‐SV reflex sensitivity in LF/TPSV can be used as a quantitative probe of baroreceptor‐cardiac reflex, similar to the baroreceptor‐heart rate reflex sensitivity in healthy subjects, and it may enable us to estimate inotropic aspect in baroreceptor‐cardiac reflex in patients with chronotropic incompetence and/or implanted pacemaker.

Heart rate variability and baroreflex function in AT2 receptor-disrupted mice.

We adapted telemetry and sequence analysis employed in humans to mice and measured heart rate variability and the spontaneous baroreflex sensitivity in angiotensin II type 2 (AT2) receptor-deleted (AT2 -/-) and wild-type (AT2 +/+) mice with either deoxycorticosterone acetate (DOCA)-salt hypertension or N(omega)-nitro-L-arginine methylester hydrochloride (L-NAME) hypertension. Mean arterial pressure leveled during the day at 101+/-1 mm Hg and during the night at 109+/-1 mm Hg in AT2 receptor-deleted mice, compared with 98+/-2 mm Hg (day) and 104+/-2 mm Hg (night) in wild-type mice. Mean arterial pressure increased in AT2 receptor-deleted mice with L-NAME to 114+/-1 mm Hg (day) and 121+/-1 mm Hg (night), compared with 105+/-2 mm Hg (day) and 111+/-2 mm Hg (night), respectively. DOCA-salt also increased day and night blood pressures in AT2 receptor-deleted mice to a greater degree than in wild-type mice. Heart rate variability in the time and frequency domain was not different between AT2 receptor-deleted mice and AT2 receptor-deleted mice at baseline. Systolic blood pressure variability in the low frequency band was lower in AT2 receptor-deleted mice (0.6+/-0.1 ms2 versus 3.9+/-1.3 ms2) than in wild-type mice. Baroreceptor-heart rate reflex sensitivity was significantly increased in AT2 receptor-deleted mice compared with wild-type mice (3.4+/-0.6 versus 2.1+/-0.5 ms/mm Hg). These differences remained after DOCA-salt and L-NAME treatments. We conclude that activation of the AT2 receptor impairs arterial baroreceptor reflex function, probably by a central action. These data support the existence of an inhibitory central effect of the AT2 receptor on baroreflex function.

Central and Baroreflex Control of Heart Rate During the Wake-Sleep Cycle in Rat

Spontaneous fluctuations in Heart Period (HP) and Mean Arterial Pressure (MAP) make it possible to evaluate baroreceptor-heart rate reflex sensitivity (BRS). 30-s sequences of HP and MAP beat-to-beat values were considered in the different wake-sleep states (Wake, W; Quiet Sleep, QS; Active Sleep, AS) in rats to assess whether 1) BRS changes between states and 2) the different indexes supply consistent BRS measures. BRS indexes were calculated according to validated literature procedures as regression coefficients of HP vs. MAP 1) within all ramps of increasing or decreasing MAP of four beats or more, with HP and MAP changing in the same direction (baroreflex-mediated fluctuations, BRSp), 2) within all such ramps irrespective of the relative direction of HP and MAP changes (baroreflex + non-baroreflex, i.e. non-homeostatic centrally driven, fluctuations, BRSA). HP vs. MAP regression coefficient along the entire 30-s sequence (bHPMAP) was also calculated. BRSp did not change among states, BRSA decreased from QS to W to AS, bHPMAP decreased from QS to W and became negative in AS. 1) as indicated by BRSp, baroreflex sensitivity is state independent, 2) BRSp to BRS(A) to bHPMAP are increasingly affected by non-baroreflex fluctuations, BRSp being most apt to measure BRS, 3) non-homeostatic MAP and HP fluctuations increase from QS to W and prevail in AS. These potentially harmful fluctuations are normally buffered by baroreflexes: in the case of baroreflex impairment, circulatory risk may arise in conditions like AS, when they prevail.

Effect of chronic volume overload on baroreflex control of heart rate and sympathetic nerve activity.

Baroreceptor-heart rate reflex sensitivity is decreased in congestive heart failure. The reflex control of heart rate and sympathetic nerve activity in rats with chronic volume overload, an established model for moderate heart failure, is still unknown. Therefore, we investigated the regulation of humoral and neuronal sympathetic activity and the baroreflex control of heart rate and sympathetic nerve activity in conscious, unrestrained rats with aortocaval shunt. Rats with aortocaval shunts had larger hearts (388 +/- 11 vs. 277 +/- 4 mg/100 g body wt), elevated central venous pressures (14 +/- 4 vs. 4 +/- 3 mmHg), and higher atrial natriuretic peptide plasma levels (87 +/- 16 vs. 25 +/- 3 pmol/l) than controls but had similar systemic blood pressure and heart rate values. Plasma epinephrine (0.63 +/- 0.16 vs. 0.21 +/- 0.08 pmol/l, P < 0.05) and norepinephrine concentrations (0.27 +/- 0.03 vs. 0.16 +/- 0.02 pmol/l, P < 0.05) were elevated in shunted rats compared with controls. Nitroprusside-induced hypotension led to a significantly greater increase in efferent splanchnic sympathetic nerve activity in shunted rats than in controls (0.9 +/- 0.1 vs. 2.6 +/- 0.6 microV, P < 0.05), whereas the heart rate responses were not different between the groups. These results indicate that the regulation of the autonomic nervous system is altered in chronically volume-overloaded rats. The arterial baroreflex control of efferent splanchnic sympathetic nerve activity was dissociated from the control of heart rate. Therefore, analysis of the activation of sympathetic nervous system assessed by direct measurements of efferent sympathetic nerve activity appears to be more sensitive for the detection of altered autonomic nervous system function than the analysis of baroreflex control of heart rate.

Modulation of baroreflex sensitivity and spectral power of blood pressure by heat stress and aging

To investigate the effects of hyperthermia and aging on baroreceptor-heart rate reflex sensitivity (BRS), cardiovascular parameters were recorded during a progressive rise in core temperature in conscious mature and senescent Fischer 344 rats. BRS was calculated from spontaneous changes in blood pressure and interbeat interval. Low- (LF, 0.01-0.20 Hz) and mid- (MF, 0.2-0.5 Hz) frequency blood pressure power were also determined. In both age groups, hyperthermia caused an increase in blood pressure, renal resistance, and LF but no changes in renal nerve activity, whereas a tachycardia was only observed in the older rats. Increases in BRS (0.80 +/- 0.14 vs. 1.72 +/- 0.34 ms/mmHg, P < 0.05) and MF (3.10 +/- 0.55 vs. 7.81 +/- 1.89 mmHg2, P < 0.05) and a positive correlation between BRS and MF (r = 0.50, P < 0.01) were observed with heating in mature but not senescent rats. These results indicate that LF, which increased with elevated core temperature, may be modulated by thermal stimuli. The augmented BRS in the mature group may contribute to the hemodynamic adjustments that occur with hyperthermia, whereas the lack of an increase in BRS during heat stress in the senescent group suggests that baroreceptor reflex modulation is impaired with aging. The positive correlation between BRS and MF in mature rats, together with the lack of an increase in renal sympathetic nerve activity, indicates that MF may reflect the modulating influence of the efferent sympathetic portion of the baroreceptor reflex loop on arterial blood pressure rather than merely the activity of the peripheral sympathetic nervous system.

Effects of moderate hypothermia on baroreflex and pulmonary chemoreflex heart rate response in decerebrate ferrets.

The effects on the baroreceptor reflexes and pulmonary reflexes of moderate immersion hypothermia (core temperature, 30.2 +/- 0.07 degrees C) have been investigated in the decerebrate ferret. Baroreflex sensitivity was estimated from the relationship between change in cardiac interval and change in systolic blood pressure following i.v. bolus injection of phenylephrine. The responses to phenylephrine in ferrets were best fitted by two linear slopes with an initial shallow slope, a, followed by a steeper slope, b. The slope or sensitivity of b was increased significantly by moderate cooling (n = 6 animals, 36 responses, P < 0.05). Pulmonary J-receptor reflex sensitivity was assessed by i.v. injection of phenylbiguanide (PBG), which evokes a dose-dependent bradycardia. The bradycardic response was unaltered by the hypothermia (n = 6 animals, 88 responses). Electrical stimulation of the right peripheral vagal nerve was employed to assess effects on the efferent components of the reflexes. The bradycardia, in response to stimulation, was significantly increased by moderate cooling at all stimulation frequencies (n = 8 animals, 88 responses, P < 0.001). Thus the results suggested that baroreceptor heart rate reflex sensitivity was enhanced by the moderate hypothermia. At least one component of the enhanced baroreflex response may be the result of changes in the efferent pathway of the reflex response. However, the absence of effect of PBG may indicate a differential afferent and efferent organization of pulmonary J-receptors compared with baroreceptors.

Relationship between cardiovascular hypertrophy and cardiac baroreflex function in spontaneously hypertensive and stroke-prone rats.

To determine whether the reduced baroreceptor-heart rate reflex sensitivity in genetically hypertensive rats is related to the level of cardiac or vascular hypertrophy. Young spontaneously hypertensive rats (SHR), stroke-prone hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats were treated chronically with the angiotensin converting enzyme (ACE) inhibitor perindopril in different regimens in order to produce a wide-ranging combination of cardiac and vascular hypertrophy. All strains were treated with perindopril (0.1, 0.3, 1 or 3 mg/kg per day) in their drinking water from 4 until 9 weeks of age. Additional groups of SHR were treated with perindopril (3 mg/kg per day) from 4 until 12 weeks and from 4 until 14 weeks of age. At 13 weeks of age all animals were chronically instrumented with arterial and venous catheters. One week later, steady-state sigmoidal mean arterial pressure-heart rate reflex curves were obtained in the conscious rats by the injection of pressor and depressor agents before and after the administration of atenolol (1 mg/kg, intravenously) to determine the vagal component. The minimum and the maximum blood pressure produced by nitroprusside and methoxamine, respectively, after simultaneous ganglion and beta-adrenoceptor blockade were used as an index of whole body vascular hypertrophy. The left ventricular to body weight ratio was measured at the end of the experiment. At 14 weeks of age, mean arterial pressure, the maximum and minimum autonomically blocked blood pressure and the left ventricular to body weight ratio were 34, 20, 9 and 17% higher, respectively, in SHR, and 56, 35, 27 and 39% higher, respectively, in SHRSP than in WKY rats. Perindopril treatment dose-dependently reduced both cardiac and vascular hypertrophy but to different extents. The highest doses reduced mean arterial pressure and the autonomically blocked maximum and minimum blood pressure in both hypertensive strains to the levels of untreated WKY rats but approximately 50% of the cardiac hypertrophy was still present. The left ventricular to body weight ratio was normalized in SHR only with the longer term perindopril treatments. A comparison of the baroreflex function curves in untreated SHR and SHRSP showed that the vagal component of the heart rate range was markedly reduced compared to that in WKY rats. Treated SHRSP had a normal mean arterial pressure and a normal autonomically blocked maximum and minimum blood pressure, but their vagal heart rate range was only 63% of that in WKY rats. The heart rate range in SHR treated from 4 to 9 weeks of age was only marginally greater than that of untreated SHR, despite prevention of hypertension and vascular hypertrophy. In SHR treated from 4 until 12 weeks of age, which prevented cardiac hypertrophy, the vagal heart rate range was markedly greater. With perindopril from the age of 4 to 14 weeks, the vagal baroreflex heart rate range was similar to that of WKY rats. Thus the improvement in the vagal heart rate range was more closely related to the prevention of cardiac hypertrophy (r = 0.73, P < 0.001) than vascular hypertrophy or a blood pressure elevation. Since there were no further changes in the indices of hypertrophy, the presence of the ACE inhibitor was likely to have been responsible for restoring the remaining 35% of the vagal baroreflex not affected by structural factors. These results suggest that prevention of cardiac rather than vascular hypertrophy is the major requirement for normalizing the vagal component of the baroreceptor-heart rate reflex in hypertensive rats. However, structural changes accounted for only about two-thirds of the vagal deficit. The remainder was restored by the presence of an ACE inhibitor, suggesting that the vagal component of the baroreceptor-heart rate reflex is normally suppressed by the renin-angiotensin system.

Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction

The baroreceptor-heart rate reflex in human is impaired 2 days after a myocardial infarction but it improves 10 days after the acute coronary event. This study investigated whether (1) the baroreceptor-heart rate reflex improvement takes the reflex back to normal, and (2) the cardiopulmonary reflex is affected by myocardial infarction. In subjects studied 8 to 11 days after a transmural anterior or inferior myocardial infarction the baroreceptor-heart rate reflex sensitivity (slope of the linear regression between negative neck chamber pressures and lengthenings in RR interval) was similar to that seen in control subjects (−6.2 ± 0.8 vs −6.0 ± 0.6 ms/mm Hg, mean ± SEM) and did not change when reassessed 10 days later. In contrast, the cardiopulmonary reflex sensitivity (changes in forearm vascular resistance induced by changing central venous pressure through nonhypotensive lower body suction and leg raising) was markedly less in subjects studied 8 to 11 days after myocardial infarction than in control subjects; the reduction amounted to 58.1 ± 8% (p < 0.01). The cardiopulmonary reflex sensitivity greatly improved when reassessed 28 to 45 days later. Thus, the baroreflex is normal about 10 days after myocardial infarction. This condition markedly impairs the cardiopulmonary reflex, but the impairment is also transient.

Medial prefrontal cortical lesions and baroreceptor heart rate reflex sensitivity in the spontaneously hypertensive rat

Previous investigations have shown that an excitotoxic lesion of the medial prefrontal cortex (MPFC) in normotensive Sprague-Dawley rats results in a reduction in the sensitivity of the baroreceptor heart rate reflex. The aim of this study was to examine the importance of the MPFC in regulation of the heart rate reflex in conscious, unrestrained spontaneously hypertensive rats (SHR). The MPFC was lesioned by bilateral microinfusions of the excitotoxin N-methyl-D-aspartic acid (NMDA). Baroreceptor heart rate reflex testing was performed by measuring reflex heart rate changes in response to blood pressure alterations induced by nitroprusside and phenylephrine with subsequent computerized sigmoidal curve-fitting of the data. Lesion of the MPFC did not significantly alter resting, systolic and diastolic blood pressure, heart rate or baro-reflex parameters (gain, thresholds, range or plateaus). These observations suggest that the putative descending facilitatory influence from the MPFC to brainstem areas, involved in baroreceptor reflex regulation observed in normotensive rats, may be defective in SHR.

Can sinoaortic baroreceptor heart rate reflex sensitivity be determined from phase IV of the Valsalva manoeuvre?

A new time related method of analysing the sinoaortic baroreceptor heart rate reflex, which determines reflex latency as well as sensitivity, was used to compare the results obtained with a phenylephrine ramp method (P) with those obtained using the whole of phase IV of Valsalva (V1) and using the phase IV systolic blood pressure overshoot alone (V2). Twenty five subjects with large ranges of age and resting blood pressures were studied. Each performed two standardised Valsalva manoeuvres and received three bolus injections of phenylephrine sufficient to cause transient pressor responses of 20-30 mmHg. Mean sensitivity values with P (6.2(3.5) ms.mmHg-1) were greater than those with V1 (4.6(2.3) ms.mmHg-1, p less than 0.001) and less than V2 (7.8(4.0) ms.mmHg-1, p less than 0.001). However, linear regression analysis showed a correlation of P with V1 (r = 0.76, p less than 0.0001) and with V2 (r = 0.80, p less than 0.0001). Reflex latency with P (1084(427) ms) was less than V1 (2416(423) ms, p less than 0.0001) and V2 (1504(441) ms, p less than 0.0005). Reflex sensitivity results obtained using phase IV of Valsalva's manoeuvre are proportionately related to phenylephrine results, but large errors were introduced into the absolute values obtained when relatively small changes were made to the method of analysis.

Estimation of sinoaortic baroreceptor heart rate reflex sensitivity and latency in man: a new microcomputer assisted method of analysis.

A new method for analysing baroreflex sensitivity has been developed. It obviates the mathematical bias inherent in earlier methods and in addition provides a direct measurement of reflex latency. Sensitivity results obtained using this method in 25 patients with a wide range of ages and resting blood pressures were similar to, but consistently lower than, those achieved with the Oxford method. Baroreflex latency results ranged from 650 to 2900 ms (mean(SD) 1084(427) ms) and were reproducible within individuals. Sensitivity results were inversely related to age and resting systolic blood pressure. Reflex latency was not related to these variables or to resting heart rate or reflex sensitivity. This method was able to identify inadequate starting data and greatly reduced the analysis time.