Baroreflex Sensitivity In Hypertension Research Articles

Closed-Loop Cardiovascular Interactions and the Baroreflex Cardiac Arm: Modulations Over the 24 h and the Effect of Hypertension

Closed-loop models of the interactions between blood pressure (BP) and heart rate variations allow for estimation of baroreflex sensitivity (feedback effects of BP changes on heart rate) while also considering the feedforward effects of heart rate on BP. Our study is aimed at comparing modulations of feedback and feedforward couplings over 24 h in normotensive and hypertensive subjects, by assessing closed-loop baroreflex models in ambulatory conditions. Continuous intra-arterial BP recordings were performed for 24 h in eight normotensive and eight hypertensive subjects. Systolic BP (SBP) and pulse interval (PI) beat-by-beat series were analyzed by an autoregressive moving average model over consecutive 6-min running windows, estimating closed-loop feedback and feedforward gains in each window. The open-loop feedback gain was estimated for comparison. Normotensive and hypertensive patients were compared during wake (18:00–22:00) and sleep (23:00–5:00) periods by a mixed-effect linear model at p < 0.05. In both groups feedback (feedforward) gain averaged values were higher (lower) in sleep than in wake. Moreover, the closed-loop feedback gain was higher in normotensive subjects both in wake and sleep, whereas the closed-loop feedforward gain was higher in hypertensive subjects during sleep. By contrast, no significant differences were found between the normotensive and hypertensive groups for the open-loop feedback gain. Therefore, the closed-loop SBP-PI model can detect circadian alterations in the feedforward gain of PI on SBP and derangements of spontaneous baroreflex sensitivity in hypertension not detectable with the open-loop approach. These findings may help to obtain a more comprehensive assessment of the autonomic dysfunction underlying hypertension and for the in-depth evaluation of the benefits of rehabilitation procedures on autonomic cardiovascular modulation.

Effects of slow breathing rate on heart rate variability and arterial baroreflex sensitivity in essential hypertension.

This study is to investigate the effects of slow breathing on heart rate variability (HRV) and arterial baroreflex sensitivity in essential hypertension.We studied 60 patients with essential hypertension and 60 healthy controls. All subjects underwent controlled breathing at 8 and 16 breaths per minute. Electrocardiogram, respiratory, and blood pressure signals were recorded simultaneously. We studied effects of slow breathing on heart rate, blood pressure and respiratory peak, high-frequency (HF) power, low-frequency (LF) power, and LF/HF ratio of HRV with traditional and corrected spectral analysis. Besides, we tested whether slow breathing was capable of modifying baroreflex sensitivity in hypertensive subjects.Slow breathing, compared with 16 breaths per minute, decreased the heart rate and blood pressure (all P < .05), and shifted respiratory peak toward left (P < .05). Compared to 16 breaths/minute, traditional spectral analysis showed increased LF power and LF/HF ratio, decreased HF power of HRV at 8 breaths per minute (P < .05). As breathing rate decreased, corrected spectral analysis showed increased HF power, decreased LF power, LF/HF ratio of HRV (P < .05). Compared to controls, resting baroreflex sensitivity decreased in hypertensive subjects. Slow breathing increased baroreflex sensitivity in hypertensive subjects (from 59.48 ± 6.39 to 78.93 ± 5.04 ms/mm Hg, P < .05) and controls (from 88.49 ± 6.01 to 112.91 ± 7.29 ms/mm Hg, P < .05).Slow breathing can increase HF power and decrease LF power and LF/HF ratio in essential hypertension. Besides, slow breathing increased baroreflex sensitivity in hypertensive subjects. These demonstrate slow breathing is indeed capable of shifting sympatho-vagal balance toward vagal activities and increasing baroreflex sensitivity, suggesting a safe, therapeutic approach for essential hypertension.

Effect of Low Dose Atorvastatin Therapy on Baroreflex Sensitivity in Hypertensives.

Impaired baroreflex function is associated with a shift in autonomic balance towards sympathetic dominance, which may play important role in the development of arterial hypertension and consequent target organ damage. To determine the effect of treatment on the cardiovascular autonomic modulation expressed by baroreflex sensitivity (BRS) in hypertensives. Atotal of one hundred fourteen hypertensive patients (58 male/56 female, 65±13years of age, BMI 30±3.4kg/m(2)) were enrolled. Control group of 20 subjects with normal blood pressure (BP) (ten male/ten female, 59±8years of age, body mass index 28.3±2.5kg/m(2)) without any treatment was also studied. BRS and BRSf were determined by the sequence and spectral method: a 5-min on-invasive beat-to-beat recording of blood pressure and R-R interval with use of Collin CBM-7000 monitor, controlled breathing at a frequency of 0.1Hz. Significant negative correlation between spontaneous BRS and BP was present in hypertensives (r=-0.52, p<0.001). All cohort of hypertensive patients had significantly lower BRS than subjects with normal blood pressure (p<0.05). The greatest decline in BRS values was in hypertensive patients with metabolic syndrome, who had BRS values <5ms/mmHg. Hypertensives with hypercholesterolaemia on low dose statin therapy (atrovastatin 20mg) had higher BRS/BRSf values than statin free patients (p<0.05). Only BRSf not BRS was significantly increased in hypertensives with beta-blockers. An inverse correlation between blood pressure and BRS is present in hypertensives. BRS and BRSf is higher in low dose statin-treated patients with essential hypertension.

Depressed Baroreflex Sensitivity in Hypertensive Rats: A Role for Reactive Oxygen Species

One of the key mechanisms in controlling blood pressure in health and disease is the baroreflex. Baroreceptors located in the carotid sinuses and aortic arch detect changes in blood pressure and trigger reflex autonomic adjustments that buffer alterations in blood pressure. In pathological conditions such as hypertension, there is impairment in the autonomic control of blood pressure resulting in changes in baroreflex sensitivity [4-6]. Indeed, compelling evidence show that the baroreflex modulation of heart rate is impaired in spontaneously hypertensive rats and patients with primary hypertension [6,7]. We have recently demonstrated that acute antioxidant therapy improves baroreflex sensitivity in models of primary (essential) and secondary hypertension [5,6]. In a model of renovascular hypertension, the 2-kidney-1-clip (2K1C), we have shown that acute treatment with Vitamin C (150 mg/Kg, i.v.), a well-known antioxidant, restored the depressed baroreflex sensitivity in those hypertensive animals [5]. Furthermore, administration of apocynin (30 µg/Kg, i.v.), a NADPH oxidase inhibitor, improved baroreflex sensitivity in the 2K1C group. In the same study, autonomic blockade with either methylatropine or propranolol reduced the changes in heart rate to the same extent in normotensive and hypertensive groups suggesting that improved baroreflex sensitivity by antioxidants were mediated by improvement in autonomic function. Taken together, those data suggest that NADPH oxidase-derived reactive oxygen species are involved in the blunted baroreflex sensitivity in secondary hypertension and that acute scavenging of superoxide restores baroreflex sensitivity. Regarding primary hypertension, we have also demonstrated in spontaneously

Cardiac Autonomic Function and Baroreflex Changes Following 4 Weeks Resistance Versus Aerobic Training in Pre Hypertensives

INTRODUCTION: Cardiac autonomic modulation and baroreflex sensitivity (BRS) are altered in individuals with hypertension. Aerobic exercise (AE) training has been shown to improve both measures, yet little is known about the effects of resistance exercise (RE). The purpose of this study was to examine heart rate variability (HRV) and baroreflex sensitivity (BRS) following 4 weeks of resistance or aerobic training in a population with high blood pressure. METHODS: Twenty-nine pre or mild hypertensives (20 males and 9 females) who were not taking any medications were recruited (Age= 48±1 yrs, systolic blood pressure (SBP) 139±2 mmHg, diastolic blood pressure (DBP) 79±1 mmHg) and randomly assigned to 4-weeks of RE (3 sets of 8 repetitions at 65% of 10RM, 3 days/week) or AE (30 minutes treadmill exercise at 65% VO2max, 3 days/week) training. Before and after training resting measures of HRV frequencies (low frequency (LF); high frequency (HF); LFHF ratio; total power (TP) and BRS were obtained. Data are presented as mean±SE. RESULTS: There was a significant decrease in resting SBP for both training modes (RE 136±3.0 pre to 132±3.4 post vs. AE 142±4.0 pre to 137±3.6 mm Hg post training, p=0.019). Also, DBP decreased significantly following both modes (RE 78±1.31 pre to 74±1.1 post vs. AE 80±1.7 pre to 77±1.6 mm Hg post, p=0.002). A significant time by mode interaction for LFHF ratio (p=0.017) with AE decreasing the ratio (275.21±67.28 to 161.26±61.49) and RE increasing this ratio (143.73±65.00 to 227.83±59.41). Natural log transformed values showed a time-by-mode interaction for lnHF (p = 0.05) as lnHF increased (4.7±0.38 to 5.4±0.35 ms2) following AE and decreased (5.98±0.37 to 5.76±0.42 ms2) following RE. BRS increased following aerobic training and decreased after resistance training (6.74±1.2 to 7.94±1.3 and 10.44±1.2 to 9.1±1.2 ms/mmHg respectively, p=0.021) CONCLUSIONS: Four weeks of AE training led to improvements of the autonomic nervous system by increasing vagal tone, and reducing the sympathovagal balance while increasing BRS in hypertensives. RE showed no improvements in cardiac autonomic tone yet decreased BRS. This suggests that aerobic training may be more beneficial in altering cardiac autonomic modulation than resistance training for individuals with pre-hypertension.

Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

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.

Heart Rate Variability and Baroreflex Sensitivity in Hypertensive Subjects With and Without Metabolic Features of Insulin Resistance Syndrome

Both abnormal autonomic control of heart rate, assessed by heart rate variability (HRV) and baroreflex sensitivity (BRS), and insulin resistance syndrome are common in hypertensive patients. It is not known, however, whether abnormalities in HRV and BRS in hypertension are related to the insulin-resistance syndrome. Therefore, we compared HRV and BRS in hypertensive subjects with and without metabolic features of the insulin-resistance syndrome. HRV was analyzed using the autoregressive method from a 45-min electrocardiographic recording (15 min lying, sitting, and standing) and BRS using the Valsalva maneuver. The groups were matched for age, sex, and antihypertensive medication, and age- and sex-matched normotensive subjects served as a control group (n = 69 in each group). The insulin-resistance syndrome was defined using the criteria of 1) hypertension (blood pressure >160/90 mm Hg), 2) hypertriglyceridemia (fasting serum triglycerides ≥2.0 mmol/L), and 3) hyperinsulinemia (fasting serum insulin ≥12 mU/L). Standard deviation of RR intervals, total, very-low-, and low-frequency power of HRV were significantly lower in hypertensive subjects with insulin-resistance syndrome compared to hypertensive subjects without the syndrome and to normotensive controls ( P < .001 for all), but the hypertensive group without the syndrome did not differ from the normotensive group. High-frequency power of HRV ( P <.01) and BRS ( P <.05) were reduced in both hypertensive groups compared to the normotensive group. In multiple regression analysis, systolic blood pressure ( P <.01) and serum triglyceride level ( P <.001) were independent predictors of reduced total power of HRV, but BRS was related only to systolic blood pressure ( P <.01). Thus, most of the abnormalities in overall HRV seem to be confined to the subgroup of hypertensive subjects with insulin-resistance syndrome, but baroreflex and respiratory modulation of heart rate are impaired also in hypertensive subjects without metabolic features of insulin-resistance syndrome.

A2 Twenty four hour baroreflex sensitivity in hypertension: The effect of a beta blocker

A2 Twenty four hour baroreflex sensitivity in hypertension: The effect of a beta blocker

Baroreflex sensitivity and heredity in essential hypertension.

Abnormalities in baroreflex control of heart rate may be important in the pathogenesis of essential hypertension. To investigate the influence of heredity on baroreflex function, we measured baroreflex sensitivity in 40 untreated patients with essential hypertension grouped by the presence (FH+) or absence (FH-) of a family history of hypertension and in 24 normotensive counterparts. Baroreflex sensitivity was assessed by both high-pressure (phenylephrine bolus) and low-pressure (amyl nitrite inhalation) stimuli. Subject groups were matched for age, blood pressure, body weight, and race. Baroreflex sensitivity (in milliseconds per millimeter of mercury) assessed by amyl nitrite inhalation was 24.3 +/- 2.8 in FH- normotensives, 12.3 +/- 1.7 in FH+ normotensives, 15.4 +/- 3.3 in FH- hypertensives, and 8.1 +/- 1.2 in FH+ hypertensives. Baroreflex sensitivity assessed by phenylephrine bolus was 28.8 +/- 5.6 in FH- normotensives, 19.3 +/- 2.8 in FH+ normotensives, 19.1 +/- 2.0 in FH- hypertensives, and 13.6 +/- 1.3 in FH+ hypertensives. Two-factor analysis of variance showed significant effects on baroreflex sensitivity for blood pressure status (normotensive versus hypertensive) and for family history of hypertension. After control line (controlling) for the effects of several variables, including age, mean arterial pressure, body weight, and race through multiple linear regression analysis, the effect of family history of hypertension on baroreflex sensitivity was still highly significant. Indeed, of all variables investigated, family history of hypertension was the strongest unique baroreflex sensitivity predictor. These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension.

Baroreflex sensitivity in hypertension during beta-adrenergic blockade.

Baroreceptor function was measured in 18 patients with essential hypertension by plotting the change in pulse interval against a phenylephrine-induced transient rise in systolic blood pressure. The influence of propranolol (160 mg daily for at least 4 weeks) on this function and on heart rate after maximal exercise was studied and correlated with the plasma propranolol level. In 13 out of the 18 patients only baroreflex resetting occurred with no change in sensitivity during propranolol administration. A definite correlation was found between the degree of beta-adrenergic blockade, expressed as the reduction in maximal exercise heart rate and the change in mean arterial pressure. No relation could be shown between plasma propranolol steady state levels and these changes. The fall in blood pressure during beta-adrenergic blockade with a low dosage of propranolol apparently does not depend on changed baroreflex sensitivity, but on the intrinsic action of this drug on beta-receptors.

Cardiovascular and respiratory changes during sleep in normal and hypertensive subjects.

The fall of blood pressure accompanying sleep in man is largely due to a diminished peripheral resistance. Subjects with normal and raised arterial pressure show qualitatively and quantitatively similar haemodynamic changes during sleep, except that the baroreflex sensitivity in hypertensives is decreased, both awake and asleep.