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PubMed2005

The concentration-dependent effects of general anesthesia on spontaneous baroreflex indices and their correlations with pharmacological gains.

Beat-to-beat assessment of spontaneously occurring fluctuations in heart rate and arterial blood pressure allows noninvasive determination of cardiovagal function, but little is known regarding the effects of general anesthesia on spontaneous baroreflex (SBR) indices. We examined (a) concentration-dependent effects of sevoflurane on SBR indices, heart rate variability (HRV), and blood pressure variability and (b) correlation and agreement between pharmacological baroreflex gains and SBR indices during sevoflurane anesthesia. Continuous electrocardiogram and invasive arterial blood pressure were monitored in nine healthy volunteers before, during, and for 3 h after sevoflurane anesthesia, during which end-tidal sevoflurane was maintained at 0.7%, 1.4%, and 2.0% in random sequences. We derived three SBR indices (sequence method, alpha-index, and low-frequency transfer function) and compared them with pressor and depressor test gains by the pharmacological method. HRV and blood pressure variability were analyzed at a fixed respiratory rate (12 breaths/min) in awake and anesthetized conditions. Except for low-frequency transfer function, SBR indices were depressed by sevoflurane and remained depressed for 30 min after emergence from anesthesia, compared with the conscious baseline value. Spontaneous sequence indices and high- and low-frequency powers of HRV demonstrated concentration-dependent depression. Pharmacological gains and SBR indices during anesthesia generally correlated well, but Bland-Altman analysis revealed that SBR indices had limits of agreement as large as the baroreflex gain itself. These data suggest that spontaneous indices are inadequate estimates of, and are inconsistent with, the pharmacological baroreflex gain during sevoflurane anesthesia.

Adult↗
PubMed2005

Baroreflex mediated control of heart rate and vascular capacitance in trout.

The baroreflex was triggered by altering branchial blood pressure with pre- and post-branchial occlusions for 30 s in rainbow trout Oncorhynchus mykiss. The cardiac limb of the baroreflex was monitored by continuous heart rate (f(H)) measurements. Responses of venous capacitance vessels were assessed, immediately following either occlusion, by measuring mean circulatory filling pressure (MCFP). Arterial responses were evaluated as the change in dorsal aortic blood pressure (P(da)) before and after pre-branchial occlusion. In untreated fish pre-branchial occlusion resulted in tachycardia (62.4+/-2.4 to 69.1+/-1.7 beats min(-1)), decreased venous capacitance reflected as an increase in MCFP (0.17+/-0.03 to 0.27+/-0.03 kPa) and increased P(da) (4.0+/-0.2 kPa compared to 3.2+/-0.1 kPa before occlusion). Post-branchial occlusion somewhat reversed the responses since f(H) decreased (62.4+/-2.4 to 53.0+/-3.1 beats min(-1)), whereas MCFP remained unaltered. Treatment with the alpha-adrenergic blocker prazosin (1 mg kg(-1)) increased resting MCFP to 0.33+/-0.03 kPa and appeared to abolish both venous and arterial responses to branchial occlusion. Subsequent atropine treatment (1.2 mg kg(-1)) abolished all chronotropic responses. We present for the first time ample evidence for baroreflex-mediated control of cardiovascular homeostasis, including both the chronotropic and the vascular limb of the baroreflex in an unanaesthetized fish. Furthermore, a novel technique to cannulate and occlude the dorsal aorta, using a Fogarty thru-lumen embolectomy catheter, is explained.

Animals↗
PubMed1999

Baroreflex sensitivity predicts the induction of ventricular arrhythmias by cesium chloride in rabbits.

Previous studies have shown that the autonomic nervous system plays an important role in the genesis of ventricular tachycardia (VT) in patients with long QT syndrome, and in cesium chloride (Cs)-induced VT in animals. The present study investigated whether baroreflex sensitivity predicts the induction of VT by Cs in the rabbit in vivo. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with the surface ECG in 27 rabbits. Rabbits were divided into 4 groups based on the Cs-induced ventricular arrhythmias: (1) no ventricular premature contractions (No-VPC group), (2) single or paired VPC (VPC group), (3) monomorphic VT (MVT group), and (4) polymorphic VT (PVT group). Baroreflex sensitivity was significantly lower in the MVT and PVT groups than in the No-VPC and VPC groups. The plasma norepinephrine concentration before Cs injection was significantly higher in the MVT group than in the other 3 groups, and the norepinephrine concentration after Cs injection was significantly higher in the MVT and PVT groups than in the No-VPC and VPC groups. Baroreflex sensitivity was negatively correlated with the norepinephrine concentration before Cs injection. These results suggest that autonomic nervous system dysfunction, as defined by reduced baroreflex sensitivity, and elevated plasma norepinephrine concentrations predict increased susceptibility to Cs-induced VT.

Animal Diseases↗
PubMed2000

Time-dependent change in baroreflex control capacity of arterial pressure by pentobarbital anesthesia in rabbits.

The present study is designed to investigate the time-dependent effect of pentobarbital anesthesia on the baroreflex arterial pressure (AP) control system in rabbits. The overall AP control capacity of the baroreflex system was assessed with mean arterial pressure (MAP) responses to the rapid mild hemorrhage (2 ml/kg body weight) and an overall open-loop gain (G) of the system. The G value was determined by means of the following formula: G = delta API/delta APS-1, where delta APl is an immediate MAP fall and delta APS a steady-state fall after the rapid hemorrhage. Prior to the experiment, two catheters for AP measurement and hemorrhage were chronically in-dwelt in the aortic arch via the left subclavian and left common carotid arteries, respectively. Control mean arterial pressure averaged for 30 sec before the rapid hemorrhage (CMAP), delta API and delta APS significantly increased and reached the maximal value at 14 min (CAMP: p < 0.01) and 28 min (delta API: p < 0.01 and delta APS: p < 0.01) after the intravenous injection of sodium pentobarbital in a 25.0 mg/kg dose, respectively. These values gradually decreased in the course of time and tended to recover to near the preanesthetic level at 77-98 min after the anesthesia. The G value significantly decreased from 7.3 in the conscious state to 1.5 at 28 min after the anesthesia (p < 0.001), gradually increased with lapse of time and recovered to near the preanesthetic level at 77-98 min after the anesthesia. No significant difference in G was observed between in the conscious and anesthetized states beyond 70 min after the anesthesia (p > 0.05). These findings suggest that pentobarbital sodium exerts a time-dependent inhibitory effect on the baroreflex system but does not significantly affect the overall AP control capacity of the baroreflex system itself at least 70 min after the intravenous administration at a dose of 25.0 mg/kg.

Adaptation, Physiological↗
PubMed2003

Oesophageal acid stimulation in humans: does it alter baroreflex function?

The aim of this study was to investigate if oesophagel acid stimulation (Bernstein test) had an influence on heart rate and blood prsure variability and baroreflex gain. We compared the cardiovascular responses in 10 patients with established gastro-esophageal reflux disease (Group 1) and 10 control subjects (Group 2) during esophageal saline and 0.1 mol/l hydrochloric acid instillation. Indices of heart rate and blood pressure variability and baroreflex gain (derived from linear spontaneous sequences and cross spectral analysis) were calculated. In Group 1 the standard deviation of RR intervals (SDRR: 46 ms vs 51 ms, p=0.030) and the root mean square of successive differences (RMSSD: 24 ms vs. 26 ms p=0.027) were significantly lower during acid infusions, than during saline. We found no significant difference in minimum, maximum and mean RR intervals and systolic blood pressures and in the percentage of RR intervals, which differed from adjacent cycles by more than 50 ms (PNN50). The power spectra of RR intervals in the high frequency band tended to be lower during acid infusion (p=0.055). There was no significant difference in blood pressure spectra, neither in low nor in high frequency band. In Group 2 there was no significant difference between any parameters measured during acid and saline. The baroreflex gain was not changed during the studied conditions in any group. Neither increased vagal tone, nor increased vagal variability occurred and the baroreflex gain was not altered during oesophageal acid simulation.

Adult↗
PubMed1999

Comparison of three methods for the determination of baroreflex sensitivity in conscious rats.

Baroreflex sensitivity was studied in the same group of conscious rats using vasoactive drugs (phenylephrine and sodium nitroprusside) administered by three different approaches: 1) bolus injection, 2) steady-state (blood pressure (BP) changes produced in steps), 3) ramp infusion (30 s, brief infusion). The heart rate (HR) responses were evaluated by the mean index (mean ratio of all HR changes and mean arterial pressure (MAP) changes), by linear regression and by the logistic method (maximum gain of the sigmoid curve by a logistic function). The experiments were performed on three consecutive days. Basal MAP and resting HR were similar on all days of the study. Bradycardic responses evaluated by the mean index (-1.5 +/- 0.2, -2.1 +/- 0.2 and -1.6 +/- 0.2 bpm/mmHg) and linear regression (-1.8 +/- 0.3, -1.4 +/- 0.3 and -1.7 +/- 0.2 bpm/mmHg) were similar for all three approaches used to change blood pressure. The tachycardic responses to decreases of MAP were similar when evaluated by linear regression (-3.9 +/- 0.8, -2.1 +/- 0.7 and -3.8 +/- 0.4 bpm/mmHg). However, the tachycardic mean index (-3.1 +/- 0.4, -6.6 +/- 1 and -3.6 +/- 0.5 bpm/mmHg) was higher when assessed by the steady-state method. The average gain evaluated by logistic function (-3.5 +/- 0.6, -7.6 +/- 1.3 and -3.8 +/- 0.4 bpm/mmHg) was similar to the reflex tachycardic values, but different from the bradycardic values. Since different ways to change BP may alter the afferent baroreceptor function, the MAP changes obtained during short periods of time (up to 30 s: bolus and ramp infusion) are more appropriate to prevent the acute resetting. Assessment of the baroreflex sensitivity by mean index and linear regression permits a separate analysis of gain for reflex bradycardia and reflex tachycardia. Although two values of baroreflex sensitivity cannot be evaluated by a single symmetric logistic function, this method has the advantage of better comparing the baroreflex sensitivity of animals with different basal blood pressures.

Analysis of Variance↗
PubMed1998

Effect of endogenous angiotensin II on renal nerve activity and its cardiac baroreflex regulation.

The effects of physiologic alterations in endogenous angiotensin II activity on basal renal sympathetic nerve activity and its cardiac baroreflex regulation were studied. The effect of angiotensin II type 1 receptor blockade with intracerebroventricular losartan was examined in conscious rats consuming a low, normal, or high sodium diet that were instrumented for the simultaneous measurement of right atrial pressure and renal sympathetic nerve activity. The gain of cardiac baroreflex regulation of renal sympathetic nerve activity (% delta renal sympathetic nerve activity/mmHg mean right atrial pressure) was measured during isotonic saline volume loading. Intracerebroventricular losartan did not decrease arterial pressure but significantly decreased renal sympathetic nerve activity in low (-36+/-6%) and normal (-24+/-5%), but not in high (-2+/-3%) sodium diet rats. Compared with vehicle treatment, losartan treatment significantly increased cardiac baroreflex gain in low (-3.45+/-0.20 versus -2.89+/-0.17) and normal (-2.89+/-0.18 versus -2.54+/-0.14), but not in high (-2.27+/-0.15 versus -2.22+/-0.14) sodium diet rats. These results indicate that physiologic alterations in endogenous angiotensin II activity tonically influence basal levels of renal sympathetic nerve activity and its cardiac baroreflex regulation.

Angiotensin II↗
PubMed2005

Circadian blood pressure variability is associated with autonomic and baroreflex-mediated modulation of the sinoatrial node.

OBJECTIVE: The day-night variability of blood pressure (BP) is of interest in the analysis of ambulatory blood pressure monitoring (ABPM). The aim of this study was to investigate whether the nocturnal BP reduction was associated with the autonomic and baroreflex-mediated modulation of the sinoatrial node in normotensive and hypertensive subjects. METHODS AND RESULTS: 63 consecutive untreated male subjects (40 hypertensive and 23 normotensive) were studied. Spectral parameters of RR interval variability and the alphaLF index (a measure of baroreflex gain) were calculated at rest. Then all the subjects performed a 24-h ABPM. RESULTS: As regards the relationships involving 24-h BP and resting heart rate (HR) and HR variability parameters, a significant correlation was found between mean RR and both systolic and diastolic nocturnal BP falls (r = 0.40, p < 0.001, r = 0.32, p < 0.01, respectively); moreover, a significant correlation was found between the nocturnal fall of systolic BP and both the LF/HF ratio and absolute power of HF (r = -0.25, p < 0.05 and r = 0.29, p < 0.05, respectively). The alphaLF index was significantly associated with the nocturnal diastolic BP fall (r = 0.26, p < 0.05) whereas the association with the systolic fall did not reach statistical significance (r = 0.23, p = 0.07). CONCLUSIONS: The relationship found between the nocturnal reduction of BP and both the LF/HF ratio and HF power of RR variability suggests that factors influencing the sympatho-vagal modulation to the heart are associated with the day-night variability of blood pressure. Moreover, the relationship between BP fall and the spontaneous baroreflex sensitivity index alphaLF, may indicate a role of the baroreflex-mediated arc function in the BP adjustments occurring during the night.

Adult↗
PubMed2002

Effects of the head-down tilt posture on postnatal development of the aortic baroreflex in the rabbit.

To clarify the effects of the head-down tilt (HDT) posture on the postnatal development of the aortic baroreflex, we raised rabbits from 3-4 weeks of age for 34-36 d in this posture, which simulates the headward shift of body fluid in space, and examined the structural and functional characteristics of the aortic nerves and baroreflex responses. The rabbits were divided into 3 different groups: 20 degrees HDT, environmental control (EC), and vivarium control (VIV). Left aortic nerve activity (ANA) at basal arterial pressure was defined as 100%, and the maximum ANA at maximal increase in arterial pressure was 265+/-103% (mean+/-SD, n=5) in the HDT, 482+/-170% (n=4) in the EC, and 677+/-491% (n=4) in the VIV groups. The minimum ANA at maximal decrease in arterial pressure was 67.3+/-13.8% in the HDT, 40.1+/-10.2% in the EC, and 38.6+/-13.8% in the VIV groups. The maximal change of ANA in response to maximal change in arterial pressure in the HDT group was significantly less than that of either the EC or VIV group (p<0.05). The average baroreflex gain in the HDT group was significantly less than in the VIV group (p<0.05). The number of unmyelinated fibers in the left aortic nerve in the HDT group was significantly less than that of each control group (p<0.05). Thus the development of the aortic baroreflex system is apparently depressed by the HDT posture, suggesting that similar consequences will be observed in mammals that develop in space.

Adrenal Glands↗
PubMed2006

Baroreflex increases correlation and coherence of muscle sympathetic nerve activity (SNA) with renal and cardiac SNAs.

Despite accumulating data of muscle sympathetic nerve activity (SNA) measured by human microneurography, whether neural discharges of muscle SNA correlates and coheres with those of other SNAs controlling visceral organs remains unclear. Further, how the baroreflex control of SNA affects the relations between these SNAs remains unknown. In urethane and alpha-chloralose anesthetized, vagotomized, and aortic-denervated rabbits, we recorded muscle SNA from the tibial nerve using microneurography and simultaneously recorded renal and cardiac SNAs. After isolating the carotid sinuses, we produced a baroreflex closed-loop condition by matching the isolated intracarotid sinus pressure (CSP) with systemic arterial pressure (CLOSE). We also fixed CSP at operating pressure (FIX) or altered CSP widely (WIDE: operating pressure +/- 40 mmHg). Under these conditions, we calculated time-domain and frequency-domain measures of the correlation between muscle SNA and renal or cardiac SNAs. At CLOSE, muscle SNA resampled at 1 Hz correlated with both renal (r(2) = 0.71 +/- 0.04, delay = 0.10 +/- 0.004 s) and cardiac SNAs (r(2) = 0.58 +/- 0.03, delay = 0.13 +/- 0.004 s) at optimal delays. Moreover,muscle SNA at CLOSE strongly cohered with renal and cardiac SNAs(coherence >0.8) at the autospectral peak frequencies, and weakly (0.4-0.5) at the remaining frequencies. Increasing the magnitude of CSP change from FIX to CLOSE and further to WIDE resulted in corresponding increases in correlation and coherence functions at nonpeak frequencies, and the coherence functions at peak frequencies remained high (>0.8). In conclusion, muscle SNA correlates and coheres approximately with renal and cardiac SNAs under closed-loop baroreflex conditions. The arterial baroreflex is capable of potently homogenizing neural discharges of these SNAs by modulating SNA at the nonpeak frequencies of SNA autospectra.

Animals↗
PubMed2004

Effect of enflurane on the baroreflex control of heart rate in decerebrate rats.

Volatile anesthetics alter the arterial baroreflex (BRX) but its mechanisms are poorly understood. This study was designed to determine the effect of 1 and 2 minimal alveolar concentrations (MAC) of enflurane on the BRX parameters in unanesthetized brain stem-intact and decerebrate rats. Under enflurane anesthesia, the femoral artery and both femoral vein were catheterized for pressor (phenylephrine) and depressor (nitroprusside) drug delivery and continuous blood pressure measurements. Decerebration was performed at midcollicular level. BRX tests were performed in 3 time periods; before enflurane (conscious brain-intact), during 1 or 2 MAC enflurane exposure 1 hour after a sham operation or a decerebration operation, and 2 hours after the termination of enflurane (zero enflurane). Mean arterial pressure (MAP) and heart rate (HR) were fitted to a sigmoid logistic equation, the Boltzman equation. The curve of best fit was obtained with a computer program. 1 MAC and 2 MAC of enflurane shifted MAP-HR baroreflex curves to the left in the all groups and significantly attenuated the baroreflex range. The slope of conscious intact period and zero enflurane period of each group did not change significantly, but during the enflurane period the slope was significantly lowered. Enflurane depressed the baroreflex sensitivity (slope) and the HR range in a similar dose-dependent manner in both brain stem-intact and decerebrate rats. Such results draw into question whether the suprapontine sites contribute to enflurane's actions on cardiovascular autonomic regulation.

Anesthetics, Inhalation↗
PubMed2000

Reduced baroreflex sensitivity in elderly humans is not due to efferent autonomic dysfunction.

A progressive decline in baroreflex sensitivity (BRS) is a characteristic feature of human aging, the basis of which is poorly understood. The purpose of the present study was to determine whether alterations in efferent baroreflex function might contribute to the age-related decrease in BRS. We studied 10 healthy young (mean age 30.5 years; age range 22-40 years; six male) and 10 healthy elderly (mean age 70.7 years; age range 67-75 years; five male) volunteers. We tested efferent cardiac vagal function using the bradycardiac response to the cold face test, and efferent sympathetic function using heart rate and blood pressure responses to four stress tests: (i) low-level cognitive stress, (ii) high-level cognitive stress, (iii) hand immersion in ice water (cold pressor test) and (iv) isometric sustained hand-grip. Haemodynamic responses to these stresses are mediated via efferent baroreflex pathways, whereas the afferent components of each reflex response are independent of afferent baroreflex pathways. BRS was measured from simultaneous Finapres-derived continuous blood pressure and digital ECG R-R interval data using the sequence analysis paradigm. As expected, BRS was significantly reduced in the elderly group (7. 29+/-0.74 ms/mmHg; mean+/-S.E.M.) compared with the young group (13. 84+/-1.13 ms/mmHg; P<0.001). However, neither the bradycardiac responses to the cold face test nor the efferent sympathetically mediated heart rate/blood pressure responses to the stress test battery were significantly different between the young and elderly groups. We conclude that the age-related decrease in BRS is not attributable to impairments in the efferent sympathetic or parasympathetic system components of the baroreceptor reflex pathway.

Adult↗
PubMed1995

Arterial baroreflex gain for muscle sympathetic nerve activity during head-up tilting in humans.

To clarify the neural mechanisms involved in blood pressure regulation during head-up tilting (HUT), arterial baroreflex controls for heart rate and muscle sympathetic nerve activity (MSNA) were evaluated by applying frequency transfer function and coherence analyses to the equidistant time series data of RR-interval, MSNA and mean blood pressure during graded HUT in six healthy subjects. Coherence analysis indicated that the RR-interval and MSNA were linked linearly with mean blood pressure in the low (0.07-0.12 Hz) and high (0.23-0.27 Hz) frequency domains. Arterial baroreflex gain for the heart rate decreased significantly during HUT, while the baroreflex gain for MSNA showed no significant change. These results indicate that the preserved arterial baroreflex gain for MSNA plays an important role in maintaining blood pressure during orthostasis.

Adult↗
PubMed2001

[Measurements of heart rate variability and baroreflex sensitivity].

BACKGROUND: Heart rate variability and baroreflex sensitivity are used to assess the activity in the autonomic nervous system. Heart rate variability is a measure of the tonic autonomic heart rate control, whereas baroreflex sensitivity measures the dynamic autonomic heart rate control. MATERIAL AND METHODS: On the basis of relevant literature and our own research, this article reviews the most commonly used techniques for measuring heart rate variability and baroreflex sensitivity, as well as results from selected studies. RESULTS: Reduced heart rate variability and reduced baroreflex sensitivity may be related to increased risk for malignant ventricular arrhythmias and sudden death in patients with coronary artery disease. These parameters are also distorted in patients with hypertension. Furthermore, heart rate variability has been suggested as a tool for monitoring anaesthesia depth. INTERPRETATION: Even though these methods are useful in pathophysiological studies of the autonomic nervous system, results from clinical studies have been diverging. Further investigation is required before these methods may be incorporated in clinical practice.

Arrhythmias, Cardiac↗
PubMed1994

Effects of aging on the arterial baroreflex control of muscle sympathetic nerve activity in healthy subjects.

To determine how arterial baroreflex gains for sympathetic nerve activity are affected by aging, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored by microneurography, and heart rate and blood pressure were recorded for the pressor or depressor responses to intravenous injections of phenylephrine or nitroglycerin in 22 healthy humans, aged 16 to 57 years old. Although the arterial baroreflex gain for the heart rate showed attenuation by aging, the gain for MSNA was not affected by aging. These data suggest a preservation of the arterial baroreflex control of sympathetic nerve activity despite attenuation of the arterial baroreflex control of the heart rate with aging in humans.

Adolescent↗
PubMed2003

[Baroreflex regulation of the cardiovascular system during hyperthermia].

Baroreflex control of human skin blood flow during hyperthermia is predominantly mediated by the stimulation of cardiopulmonary low pressure baroreceptors. Under hyperthermic conditions, the active cutaneous vasodilator system represents an efferent arm of the baroreflex, when baroreceptor unloading elicits withdrawal of sympathetic active vasodilator activity. Splanchnic sympathetic nerve activity is not likely modulated by the arterial and cardiopulmonary baroreceptors during hyperthermia. Little is known regarding the effects of heat stress on baroreflex control of the heart rate and on the vascular resistance. Baroreflex control of heart rate during heat stress seems to be dependent on the species of experimental animals and on their age.

Animals↗
PubMed2004

Baroreflex failure: a neglected type of secondary hypertension.

The arterial baroreflex buffers abrupt transients of blood pressure and prevents pressure from rising or falling excessively. In experimental animals, baroreceptor denervation results in temporary or permanent increases in blood pressure level and variability, depending on the extent of denervation. In humans, the clinical syndrome of baroreflex failure may arise from denervation of carotid baroreceptors following carotid body tumour resection, carotid artery surgery, neck irradiation and neck trauma. The syndrome is characterised by acute malignant hypertension and tachycardia followed by labile hypertension and hypotension. Baroreflex failure can be a cause of hypertension and should also be considered in the differential diagnosis of pheochromocytoma. Patients with suspected baroreflex failure should be referred to specialised centres for diagnostic testing and treatment.

Animals↗
PubMed2005

Age-dependent relationship between the carotid intima-media thickness, baroreflex sensitivity, and the inter-beat interval in normotensive and hypertensive subjects.

The interrelationship between baroreflex sensitivity expressed in ms/mm Hg (BRS) or in Hz/mm Hg (BRSf), carotid wall thickness (IMT), and age was investigated in hypertensive and normotensive subjects with respect to the mean inter-beat interval (IBI) and blood pressure (BP). BP monitoring was performed in 25 treated hypertensives (Hy; 47.4+/-9.2 years of age) and 23 normotensives (Norm; 44.5+/-8.1 years). IMT was measured by ultrasonography. BRS and BRSf were determined by the spectral method (five-minute non-invasive beat-to-beat recording of BP and IBI, Finapres, controlled breathing at a frequency of 0.33 Hz). Significant differences between Hy and Norm were detected in IMT (Hy: 0.624+/-0.183, Norm: 0.522+/-0.070 mm; p<0.01), BRS (Hy: 3.5+/-1.6, Norm: 5.7+/-2.3 ms/mm Hg; p<0.01), BRSf (Hy: 0.005+/-0.002, Norm: 0.009+/-0.004 Hz/mm Hg; p<0.01), systolic BP (Hy: 131+/-21, Norm: 116+/-17 mm Hg; p<0.01) and diastolic BP (Hy: 77+/-16, Norm: 64+/-12 mm Hg; p<0.01). A significant correlation was found between age and IMT (Norm: 0.523, p<0.05; Hy+Norm: 0.419, p<0.01), age and BRS (Norm: -0.596, p< 0.01; Hy+Norm: -0.496, p<0.01), age and BRSf (Norm: -0.555, p<0.01; Hy: -0.540, p <0.01; Hy+Norm: -0.627, p<0.01), age and IBI (Hy: 0.478, p<0.05), age and diastolic BP (Hy: -0.454, p<0.05), BRS and IMT (Hy+Norm: -0.327, p<0.05) and BRSf and IMT (Hy+Norm: -0.358, p<0.05). Hypertensive patients have increased IMT and decreased BRS and BRSf. The positive correlation between age and IMT and the negative correlation between age and BRS and BRSf are in agreement with the hypothesis that the age-dependent decrease of baroreflex sensitivity corresponds to the age-related structural changes of the carotid wall. Using two indices of baroreflex sensitivity, BRS and BRSf, we could show that baroreflex sensitivity in hypertensives is lower not only due to thickening of the carotid wall, but also due to aging.

Adult↗