Component Of Systolic Blood Pressure Research Articles

Cardiorespiratory synchronisation and systolic blood pressure correlation of peripheral arterial stiffness during endoscopic thoracic sympathectomy

Muscle sympathetic nerve activity (MSNA) is known as an effective measure to evaluate peripheral sympathetic activity; however, it requires invasive measurement with the microneurography method. In contrast, peripheral arterial stiffness affected by MSNA is a measure that allows non-invasive evaluation of mechanical changes of arterial elasticity. This paper aims to clarify the features of peripheral arterial stiffness to determine whether it inherits MSNA features towards non-invasive evaluation of its activity. To this end, we propose a method to estimate peripheral arterial stiffness beta at a high sampling rate. Power spectral analysis of the estimated beta was then performed on data acquired from 15 patients (23.7 pm 9.0 years) who underwent endoscopic thoracic sympathectomy. We examined whether beta exhibited the features of MSNA where its frequency components synchronise with heart and respiration rates and correlates with the low-frequency component of systolic blood pressure. Regression analysis revealed that the local peak frequency in the range of heartbeat frequency highly correlate with the heart rate (R^{2}=0.85, p=6.3times 10^{-13}) where the regression slope was approximately 1 and intercept was approximately 0. Frequency analysis then found spectral peaks of beta approximately 0.2 Hz that correspond to the respiratory cycle. Finally, cross power spectral analysis showed a significant magnitude squared coherence between beta and systolic blood pressure in the frequency band from 0.04 to 0.2 Hz. These results indicate that beta inherits the features observed in MSNA that require invasive measurements, and thus beta can be an effective non-invasive substitution for MSNA measure.

Facial Distances and Possible Risk of High Blood Pressure: The Analyses of Young and Middle‐ Aged Adult Populations of Northern Nigeria

The objectives of the study were to determine the relationship between the facial distances and blood pressure across different age groups of young adults and middle‐aged population in males and females of northern Nigeria. Secondly, to determine the best facial predictors and discriminators of the blood pressure in the study population. Participants included 397 males and 159 females of northern of Nigeria with mean age of 25.37± 7.78 years. The facial distances were measured using direct anthropometry and blood pressure was determined using standard protocols. Pearson's correlation, step–wise multiple linear regression and receiver operating characteristic curve were employed to analyze the data. Measurements of blood pressure were in mmHg, age in years, bmi in kg/m2 and the remaining facial distances in mm. It was observed that no significant correlation between the facial distances and blood pressure (BP) in younger adult males and females except for lower facial height (LFH) and diastolic BP in males. Above the age of 30 years, significant correlation was noticed between the right ear width (EW), left EW, head length (HL) with both systolic and diastolic BP. The nasal length (NL) and nasal width (NW) correlated significantly with systolic and diastolic BP respectively in males only. For females, bizygomatic distance (BD) correlated only with systolic BP. The best predictors of systolic BP were left EW and HL in males and females respectively, while the best predictors of diastolic BP were left EW and right EW in males and females respectively. LFH was found to predict only the systolic blood pressure component in younger male adults. The best discriminating potential of facial distances with regard to abnormal blood pressure was only observed in the middle‐aged population. In both sexes right EW and left EW had more than 80% discriminating ability of abnormal BP (area under curve > 0.80). However, head width (HW) and HL had more than 80% discriminating ability of abnormal BP in males and females respectively. In conclusion, a significant correlation was observed between the facial distances and BP in middle‐ aged adult population. The facial soft tissue gave best predictors and discriminator in both sexes.Support or Funding InformationNoneThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effect of spinal manipulative treatment on cardiovascular autonomic control in patients with acute low back pain

BackgroundThis study aimed to quantify the effect of spinal manipulative treatment (SMT) from an analysis of baroreflex, systolic blood pressure and heart rate variability (HRV) on patients with acute back pain. It was hypothesized that SMT would increase the parasympathetic cardiovascular autonomic control.MethodsTwenty-two patients with acute back pain were randomly divided into two groups: one receiving sham treatment (Sham) and the other receiving SMT. Recordings were completed during the first day and the seventh day, immediately before and after treatment on both days. ECG and systolic blood pressure were continuously recorded to compute cardiovascular variability and baroreflex sensitivity components. The perceived level of pain was measured with the numeric pain scale (NPS) 48 h before, just before and just after each treatment. The NPS ranged from 0 to 100% (peak of pain before treatment). ECG and systolic blood pressure recordings were analyzed in time frequency domain using the Smoothed pseudo Wigner-Ville distribution.ResultsRoot mean square of the successive differences, high frequency power of the heart rate variability, and high frequency baroreflex sensitivity differences between post and pre tests were higher in the SMT group than in the Sham group (p < 0.01), whereas no differences were observed with the other heart rate variability components. Also, no differences were observed with the systolic blood pressure components. Although the estimated pain scale values decreased over time, no difference was observed between the SMT and Sham groups.ConclusionsThis seems to be the first study to assess the effect of SMT on both heart rate variability and baroreflex sensitivity in patients with acute back pain. SMT can be seen to provoke an increase in parasympathetic control known to relate to a person’s healthy state. Thus, cardiovascular variability analysis may be a useful tool for clinicians to quantify and objectify the beneficial effects of spinal manipulation treatment.

Tractographic analysis of the medulla oblongata necessitates partial re‐wiring of the contemporary neural circuit for baroreflex‐mediated sympathetic vasomotor tone

Contemporary dogma stipulates that the caudal ventrolateral medulla (CVLM) participates in baroreflex‐mediated sympathetic vasomotor tone by acting as a synaptic relay that connects the nucleus tractus solitarii (NTS) to the rostral ventrolateral medulla (RVLM). Functionally, CVLM exerts an inhibitory action on RVLM neurons that are involved in tonic and reflex control of sympathetic vasomotor tone. Whether neuronal traffic in the above‐mentioned circuit actually takes place in the brain stem during the execution of baroreflex has never been visualized. This study was undertaken to fill this void. In male adult C57BL/6 mice instrumented for physiological measurements by radiotelemetry, intracerebroventricular (i.c.v.) infusion of angiotensin (7.5 μg/h at 0.5 μL/h) by osmotic minipump for 7 days elicited a significant elevation in mean arterial pressure (MAP) that returned to basal levels over time. Determined by the power density of the low‐frequency component of systolic blood pressure, the baroreflex‐mediated sympathetic vasomotor tone exhibited a significant increase that paralleled temporally the elevation in MAP. Tractographic analysis based on magnetic resonance imaing/diffusion tensor imaging (DTI) of the medulla oblongata using a 9.4T scanner further revealed that under basal MAP, there was robust connectivity between the NTS and RVLM. This NTS‐RVLM connectivity was substantially reduced when visualized during sustained hypertension and elevated baroreflex‐mediated sympathetic vasomotor tone. More importantly, the connectivity between the NTS and RVLM was re‐established when MAP or low‐frequency power returned to their basal levels. Quantification of the magnitude of NTS‐RVLM connectivity by two DTI indices, fractional anisotropy (FA) and number of fiber tracts, yielded comparable results. Interestingly, in an anterior‐posterior presentation of the FA map of the medulla oblongata, we rarely (P &lt; 0.0001, Chi‐square analysis) detected the obligatory presence of connectivity between NTS and CVLM under basal conditions (3 out of 56 observations) or during neurogenic hypertension (1 out of 28 observations). Our visualization of the baroreflex at work therefore necessitates partial re‐wiring of the circuit for baroreflex‐mediated sympathetic vasomotor tone.

Increased expression of angiotensin II type 2 receptors in the solitary-vagal complex blunts renovascular hypertension.

Angiotensin II increases and decreases arterial pressure by acting at angiotensin type 1 and type 2 receptors, respectively. Renovascular hypertensive rats exhibit a high level of activity of the peripheral and central renin-angiotensin system. Therefore, in the present study, we evaluated the effect of increasing the expression of angiotensin type 2 receptors in the solitary-vagal complex (nucleus of the solitary tract/dorsal motor nucleus of the vagus), a key brain stem region for cardiovascular regulation, on the development of renovascular hypertension. Holtzman normotensive rats were implanted with a silver clip around the left renal artery to induce 2-kidney 1-clip renovascular hypertension. Three weeks later, rats were microinjected in the solitary-vagal complex with either an adenoassociated virus to increase the expression of angiotensin type 2 receptors or with a control vector. We observed that increasing angiotensin type 2 receptor expression in the solitary-vagal complex attenuated the development of renovascular hypertension and also reversed the impairment of the baroreflex and the increase in the low-frequency component of systolic blood pressure observed in renovascular hypertensive rats. Furthermore, an observed decrease in mRNA levels of angiotensin-converting enzyme 2 in the solitary-vagal complex of renovascular hypertensive rats was restored to control levels after viral-mediated increases in angiotensin type 2 receptors at this site. Collectively, these data demonstrate specific and beneficial effects of angiotensin type 2 receptors via the brain of hypertensive rats and suggest that central angiotensin type 2 receptors may be a potential target for therapeutics in renovascular hypertension.

Revealing the role of the autonomic nervous system in the development and maintenance of Goldblatt hypertension in rats

Despite extensive use of the renovascular/Goldblatt model of hypertension—2K-1C, and the use of renal denervation to treat drug resistant hypertensive patients, autonomic mechanisms that underpin the maintenance of this hypertension are important yet remain unclear. Our aim was to analyse cardiovascular autonomic function by power spectral density analysis of both arterial pressure and pulse interval measured continuously by radio telemetry for 6 weeks after renal artery clipping. Mean arterial pressure increased from 106 ± 5 to 185 ± 2 mm Hg during 5 weeks post clipping when it stabilized. A tachycardia developed during the 4th week, which plateaued between weeks 5 and 6. The gain of the cardiac vagal baroreflex decreased immediately after clipping and continued to do so until the 5th week when it plateaued (from − 2.4 ± 0.09 to − 0.8 ± 0.04 bpm/mm Hg; P < 0.05). A similar time course of changes in the high frequency power spectral density of the pulse interval was observed (decrease from 13.4 ± 0.6 to 8.3 ± 0.01 ms2; P < 0.05). There was an increase in both the very low frequency and low frequency components of systolic blood pressure that occurred 3 and 4 weeks after clipping, respectively. Thus, we show for the first time the temporal profile of autonomic mechanisms underpinning the initiation, development and maintenance of renovascular hypertension including: an immediate depression of cardiac baroreflex gain followed by a delayed cardiac sympathetic predominance; elevated sympathetic vasomotor drive occurring after the initiation of the hypertension but coinciding during its mid-development and maintenance.

Causes of autonomic dysfunction in idiopathic recurrent kidney stone formers

A higher prevalence of hypertension and adverse cardiovascular outcomes has been reported in kidney stone formers (KSF). We performed this study with the purpose of evaluating the autonomic nervous system (ANS) activity in KSF. We performed a 70° head-up tilt test in 30 idiopathic recurrent KSF aged 45.6 ± 12.1 years old (17 men: 13 women) and 30 healthy controls aged 42.0 ± 12.4 years old (17 women: 13 men). Thirteen KSF were hypertensive, and 17 were normotensive. Blood pressure (BP) and heart rate variability (HRV) were used for the non-invasive assessment of the efferent activity of the ANS. Discrete wavelet transform (DWT) was used to quantify the low-frequency (LF: 0.04-0.15 Hz) and high-frequency (HF: 0.15-0.4 Hz) components during several periods of tilt. The results showed significantly higher HR and BP in KSF, in both supine and tilt positions. DWT revealed diminished HRV in the kidney stone patients during head-up tilt, with no increase in the LF and greater decrease in the HF components. The differences in the HF component of HRV were associated with obesity and hyperuricosuria, but the abnormalities of the LF component were independent of the explanatory variables. The LF component of systolic BP was significantly higher in KSF and was associated with hypertension. Several factors may contribute to the presence of autonomic dysfunction in patients with recurrent nephrolithiasis. This abnormality has significant implications in cardiovascular risk assessment and treatment planning.

Spectral analysis of muscle sympathetic nerve activity in heat-stressed humans.

Whole body heating increases muscle sympathetic nerve activity (MSNA); however, the effect of heat stress on spectral characteristics of MSNA is unknown. Such information may provide insight into mechanisms of heat stress-induced MSNA activation. The purpose of the present study was to test the hypothesis that heat stress-induced changes in systolic blood pressure variability parallel changes in MSNA variability. In 13 healthy subjects, MSNA, electrocardiogram, arterial blood pressure (via Finapres), and respiratory activity were recorded under both normothermic and heat stress conditions. Spectral characteristics of integrated MSNA, R-R interval, systolic blood pressure, and respiratory excursions were assessed in the low (LF; 0.03-0.15 Hz) and high (HF; 0.15-0.45 Hz) frequency components. Whole body heating significantly increased skin and core body temperature, MSNA burst rate, and heart rate, but not mean arterial blood pressure. Systolic blood pressure and R-R interval variability were significantly reduced in both the LF and HF ranges. Compared with normothermic conditions, heat stress significantly increased the HF component of MSNA, while the LF component of MSNA was not altered. Thus the LF-to-HF ratio of MSNA oscillatory components was significantly reduced. These data indicate that the spectral characteristics of MSNA are altered by whole body heating; however, heat stress-induced changes in MSNA do not parallel changes in systolic blood pressure variability. Moreover, the reduction in LF component of systolic blood pressure during heat stress is unlikely related to spectral changes in MSNA.

Post-exercise recovery of autonomic cardiovascular control: a study by spectrum and cross-spectrum analysis in humans.

The recovery of the baseline autonomic control of cardiovascular activity after exercise has not been extensively studied. In 12 healthy subjects, we assessed the time-course of recovery by autoregressive spectrum and cross-spectrum analysis of heart period and systolic blood pressure during the 3 h after the end of 20 min of steady-state exercise at 50% (light workload, LW) and 80% (moderate workload, MW) of the individual's anaerobic threshold. The electrocardiogram and non-invasive blood pressure were simultaneously recorded during 10 min periods in the sitting position, at rest before exercise, and at 15, 60 and 180 min of recovery after exercise. At 15 min we observed a persistent tachycardia and relative hypotension; after MW, at 60 min heart rate was still slightly higher. Spectrum and cross-spectrum analysis showed, at 15 min, an increase in the low frequency component of systolic blood pressure, a reduction in the high frequency component of heart rate (larger in MW), and a decrease in baroreceptor sensitivity. After 60 and 180 min none of these parameters was significantly different from those at rest, although, in MW, some subjects still displayed signs of sympathetic activation after 1 h. We concluded that, after 15 min of recovery, the cardiovascular reflexes were blunted, that sympathetic nerve activity was still enhanced, and that the tone in the vagus had not fully recovered. Only the persistent vagal restraint seemed to be exercise intensity-dependent. For complete restoration of autonomic control after LW 1 h of rest was sufficient, and just enough after MW.

Subarachnoid haemorrhage-induced sympathoexcitation in rats is reversed by bosentan or sodium nitroprusside.

1. The roles played by nitric oxide (NO) and endothelin (ET) in the genesis of sympathetic nervous activation following experimental subarachnoid haemorrhage was investigated using spectral analysis of blood pressure rhythms. 2. Subarachnoid haemorrhage was induced in conscious rats by injecting 0.3 mL homologous blood via a catheter placed along the surface of the brain and directed towards the circle of Willis. Three hours after the insult and after sympathetic activation was evident, animals received either an acute injection of the ET antagonist bosentan (5 mg/kg, i.v.; n = 7), an infusion of the NO donor sodium nitroprusside (SNP; 18 microg/h; n = 7) or no treatment (n = 7). 3. Three hours following the induction of subarachnoid haemorrhage, the mid-frequency components of systolic blood pressure were markedly elevated, indicating a pronounced sympathoexcitation. However, blood pressure and heart rate levels remained unchanged at this time. In the absence of treatment, the mid-frequency components of blood pressure remained elevated for a subsequent 2 h. Treatment with a non-hypotensive dose of SNP reversed the sympathoexcitation within 1 h. Treatment with bosentan was also effective in reducing the mid-frequency oscillations in blood pressure associated with subarachnoid haemorrhage. 4. Our results indicate that subarachnoid haemorrhage is associated with an acute activation of the sympathetic nervous system. The degree of sympathoexcitation can be reversed by the use of either bosentan or SNP.

Effects of autonomic disruption and inactivity on venous vascular function.

The effects of autonomic disruption and inactivity were studied on the venous vascular system. Forty-eight subjects, 24 with spinal cord injury (SCI) and 12 sedentary and 12 active able-bodied controls, participated in this study. Peripheral autonomic data were obtained to estimate sympathetic vasomotor control [low-frequency component of systolic blood pressure (LF(SBP))]. Vascular parameters were determined using strain-gauge venous occlusion plethysmography: venous capacitance (VC), venous emptying rate (VER), and total venous outflow (VO(t)). An additional vascular parameter was calculated: venous compliance [(VC/occlusion pressure) x 100]. VC and VO(t) were significantly different (SCI < sedentary < active). VER adjusted for VC was not different for any group comparison, whereas venous compliance was significantly lower in the SCI group than in the able-bodied groups and in the sedentary group compared with the active group. Regression analysis for the total group revealed a significant relationship between LF(SBP) and venous compliance (r = 0.64, P < 0.0001). After controlling for LF(SBP) through analysis of covariance, we found that mean differences for all venous vascular parameters did not change from unadjusted mean values. Our findings suggest that in subjects with SCI, the loss of sympathetic vasomotor tone contributes more than inactivity to reductions in venous vascular function. Heightened VC, VO(t), vasomotor tone, and venous compliance in the active group compared with the sedentary group imply that regular endurance training contributes to optimal venous vascular function and peripheral autonomic integrity.

Contribution of the renin-angiotensin and kallikrein-kinin systems to short-term variability of blood pressure in two-kidney, one-clip hypertensive rats

Spectral analysis was recently chosen to characterize the fast oscillations, depending on the autonomic nervous system, in heart rate and blood pressure variabilities. Humoral stimuli could impinge on the low-frequency domain of blood pressure variability since the time lag to humoral system activation is greater. This study was designed to analyse low-frequency components of short-term variability of blood pressure of conscious rats in conditions where humoral systems were activated. We studied rats with two-kidney, one-clip Goldblatt hypertension in which the blood pressure level was dependent upon the renin-angiotensin and kallikrein-kinin systems. Spectral powers of the systolic and diastolic blood pressure and heart rate were computed in the high (respiratory)-, mid (0.2–0.6 Hz)- and low (0.02–0.2 Hz)-frequency bands, as detected by the fast Fourier transform technique in consecutive 102-s stationary periods. Hypertensive rats exhibited a marked low-frequency component of systolic (+ 261%) and diastolic (+ 169%) blood pressure variabilities when compared to sham-operated animals. First, losartan, a selective non-peptide angiotensin AT 1 receptor antagonist, reduced this low-frequency component (− 44% and − 25% for systolic and diastolic blood pressure). In a second series of hypertensive rats, HOE 140, d-Arg-[Hyp 3,Thi 5, d-Tic 7,Oic 8]bradykinin, a bradykinin B 2 receptor antagonist, decreased the low-frequency component of systolic (− 28%) and diastolic (− 40%) blood pressure. Losartan, added after HOE 140, induced a supplementary decrease of the low-frequency component (− 60% and − 42% for systolic and diastolic blood pressure). After the combined blockade, the low-frequency components of systolic and diastolic blood pressure variabilities of the hypertensive rats were equivalent to those of the control rats. Two-kidney, one-clip hypertension was also associated with an elevation of the mid-frequency component of the systolic blood pressure (+ 55%). The administration of HOE 140 did not change this component while losartan, alone or added after HOE 140, led to an increase (around + 100%) in mid-frequency oscillations of systolic blood pressure. The high-frequency oscillations of systolic blood pressure were increased by losartan in the two series of hypertensive rats. Losartan increased the mid-frequency component of heart rate variability in sham-operated rats while the heart rate variability was not modified during any of the treatment periods in two-kidney, one-clip rats. In conclusion, an increase in the low-frequency component of blood pressure variability was observed in a model of hypertension where the blood pressure is dependent upon humoral activities. The reduction of the slow fluctuations following the combined blockade of the kallikrein-kinin and the renin-angiotensin systems suggested the contribution of these humoral systems to this low-frequency component of blood pressure variability.

The mechanism of blood pressure variability. Study in patients with fixed ventricular pacemaker rhythm.

Several studies have shown that heart rate variability plays an anti-oscillatory role in the regulation of blood pressure variability in humans. We tested whether systolic blood pressure variability in patients with a fixed ventricular pacemaker rhythm differs from that in patients with sinus rhythm. In 18 patients with a fixed ventricular pacemaker rhythm and in ten age-matched patients with sinus rhythm the systolic blood pressure oscillation and the low and high-frequency spectral components of systolic blood pressure were studied in the resting supine position during spontaneous breathing and during forced deep ventilation of 6 cycles.min-1. Patients with a pacemaker had a higher amplitude of systolic blood pressure oscillation than control subjects during spontaneous breathing (13.5 +/- 2.0 mmHg vs 6.4 +/- 1.6 mmHg, P = 0.035), and a slight but not significant difference also persisted during forced deep ventilation 19.0 +/- 2.3 mmHg vs 15.0 +/- 2.3 mmHg, P = 0.18). The increment in systolic blood pressure fluctuation from spontaneous breathing to forced deep ventilation was less marked in the pacemaker group than in the control subjects (40% vs 130%, P = 0.43). Although all the systolic blood pressure spectral components of the pacemaker patients were higher during both spontaneous breathing and forced deep ventilation, the differences between the two groups did not reach statistical significance. Our observations in patients with a fixed ventricular pacemaker rhythm suggest that the mechanical effects on the intrathoracic vessels and the consecutive stroke volume changes are responsible for respiration-related systolic blood pressure oscillation and reflex systolic blood pressure changes.

Power spectral analysis of heart rate and blood pressure variability in lumbar epidural anaesthesia

The purpose of this study was to evaluate autonomic nervous system activity during high and low lumbar epidural anaesthesia. Ten patients undergoing lower limb surgery with lumbar epidural anaesthesia (low epidural anaesthesia group; mean upper dermal block level, T10.7 +/- 1.1), and ten patients undergoing either abdominal total hysterectomy or inguinal hernia under lumbar epidural anaesthesia (high epidural anaesthesia group; mean upper dermal block level, T5.1 +/- 1.0). Ten healthy volunteers were used as the control group. The autonomic nervous system activity was measured by heart rate and blood pressure variability with power spectral analysis. For the analysis of heart rate variability, frequency components were divided into two factors, a low frequency component RR (LFCRR: 0.03 Hz-0.15 Hz) that mediated sympathetic and parasympathetic activity and a high frequency component RR (HFCRR: 0.15 Hz-0.4 Hz) that mediated parasympathetic activity. In the analysis of blood pressure variability, the frequency components were also divided into two factors; a low frequency component of systolic blood pressure and diastolic blood pressure (LFCSBP and LFCDBP: 0.03 Hz-0.15 Hz) that was mediated by peripheral sympathetic vasomotor activity and a higher frequency component of systolic blood pressure and diastolic blood pressure (HFCSBP and HFCDBP: 0.15 Hz-0.4 Hz) that was mediated by a mechanical consequence of respiration. There were no changes in heart rate variability during epidural anaesthesia. However, LFCSBP and LFCDBP decreased in high epidural anaesthesia (P < 0.01). On the contrary, LFCSBP increased in low epidural anaesthesia (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)