Decreased Baroreceptor Sensitivity Research Articles

Modeling and Analysis of Central and Peripheral Autonomic Contributions to Decreased Cardiac Vagal Tone Following Myocardial Infarction

Loss of cardiac function following myocardial infarction is accompanied by neural adaptation in baroreflex systems that are compensatory in the short term but then become associated with long-term disease progression. A hallmark of these baroreflex changes is decreased vagal tone. The closed-loop feedback structure of the baroreflexes confounds the source of decreased vagal tone following myocardial infarction (MI). We recognize that in a feedback network causality is distributed in the network interactions, and so explore the effects of MI on the potential contribution to vagal withdrawal of each neural component of our previously published closed-loop baroreflex computational model. The model is composed of differential equations representing the blood flow through various body compartments and sigmoidal functions to represent the saturating firing behavior of neurons. Neuronal adaptations leading to decreased vagal activity could occur in various neuronal groups located centrally in the brainstem. Adaptations could also occur peripherally at the baroreceptors or the heart’s “little brain”, the intrinsic cardiac nervous system. We developed five alternative models to reflect these hypotheses. Of the alternative models, only the model representing adaptation in the baroreceptors predicted both physiological baroreflex function and a decrease in vagus nerve activity. These findings suggest that decreased vagal activity after myocardial ischemia may be due, at least in part, to a decrease in baroreceptor sensitivity. We also link these model predictions with experimental evidence from the literature. NIH U01-HL133360, NIH OT2-OD030534, NSF 1940700, and NSF OAC-1919839. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Sleep duration and disturbance are associated with orthostatic heart rate recovery: Findings from the Irish Longitudinal Study on Ageing

ObjectiveTo examine a novel measurement of autonomic innervation, the early heart rate response to orthostasis, in relation to sleep duration and disturbance (actigraphy-based and self-reported) in healthy older adults. DesignCross-sectional analyses of a nationally representative prospective cohort study, the Irish Longitudinal Study on Ageing (TILDA). ParticipantsNine hundred sixty community-dwelling adults aged 50 and over (mean age 65.6 ± 8.1; 53% women). MeasurementOrthostatic heart rate response was measured during an active stand test. Beat-to-beat heart rate was monitored over 3 minutes using noninvasive digital photoplethysmography. Mean values at each 10-second time point after standing were generated and differences from baseline at each time point were used for analysis. Actigraphy-based sleep measures were extracted from wrist-worn GENEactiv devices; self-reported sleep measures using interview questions. ResultsLinear mixed-effects regression analyses, with inclusion of a large number of confounders, show that self-reported sleep duration and actigraphy-based sleep duration and disturbance were associated with altered orthostatic heart rate response, particularly within the first 20 seconds poststanding. Self-reported short sleep (β = -0.06; 95% confidence interval [CI]: -0.11, -0.01) and long sleep (β = -0.15; 95% CI: -0.24, -0.05) and actigraphy-based short sleep (β = -0.08; 95% CI: -0.14, -0.01) were characterized by a smaller increase at 10 seconds (p < .01). Actigraphy-based short sleep (β = 0.15; 95% CI: 0.08, 0.22) and sleep disturbance (β = 0.04; 95% CI: 0.02, 0.06) were associated with a slower return toward baseline at 20 seconds (p < .001). ConclusionsOur findings suggest sympathetic dysregulation, impaired vagal reactivation, and/or decreased baroreceptor sensitivity in the presence of shortened or disturbed sleep.

Central arterial stiffness, wave reflection, and heart rate variability following 4-week high-intensity resistance training intervention in young active women.

Arterial stiffness, expedited wave reflection, and autonomic dysfunction are risk factors for cardiovascular disease, which is the leading cause of death in women in the United States. Evaluation of the effects of resistance training on these factors has been inconclusive, and even less is known about the effects of high-intensity resistance training (HIRT). This study evaluated the effects of a 4-week HIRT intervention on central arterial stiffness, wave reflection, and heart rate variability in young healthy and active women. 9 women were recruited and underwent a 4-week control period followed by the intervention. Measurements were recorded pre-control, post-control/pre-intervention, and post-intervention. There were no significant changes to central arterial stiffness, wave reflection, or heart rate variability. There was a significant increase in resting heart rate (bpm: 62 ± 7, 66 ± 10; p = 0.003) and a significant decrease in baroreceptor sensitivity (30 ± 7, 21 ± 7; p = 0.018) pre- to post-intervention. There was a significant decrease in total peripheral resistance pre- to post-intervention (1.076 ± 0.281, 0.916 ± 0.250; p = 0.002). Squat, bench press, and deadlift increased pre- to post-intervention (kg: 62 ± 11, 71 ± 9, p = 0.000; 37 ± 7, 40 ± 7, p = 0.002; 76 ± 19, 84 ± 19, p = 0.000). 4weeks of HIRT can supplement a healthy lifestyle in women by increasing strength while decreasing peripheral resistance and preserving arterial pressures. Further evaluation is necessary to investigate the observed increase in resting heart rate and decrease in baroreceptor sensitivity and to determine long-term effects of this training.

Cardiovascular sequelae of sports-related concussions.

We are becoming more aware of sports-related concussions (SRCs). Current return-to-play (RTP) guidelines are often based on subjective clinical symptoms rather than objective physiologic measures. Although evidence is limited, the purpose of this article is to summarize the data pertaining to acute and chronic cardiovascular effects of SRCs, and to determine whether there are objective metrics that could improve currently used RTP protocols. Research shows that SRCs cause cardiovascular autonomic nervous system (CV-ANS) dysfunction induced by decreased baroreceptor sensitivity (BRS). This disturbance persists past the point of clinical symptom resolution and can worsen through subsequent exertion, which may impact long-term recovery. Further studies are needed to establish the most appropriate physiologic metrics for analyzing recovery post-SRC and whether the addition of physiologic measures to RTP guidelines improves recovery from these injuries. This is an understudied area that carries important clinical implications. Larger and more robust trials are warranted to inform the development of guidelines that should focus on lessening the compounding effects of multiple concussions and improve the management of SRCs.

Increased fibroblast growth factor-21 in chronic kidney disease is a trade-off between survival benefit and blood pressure dysregulation

Circulating levels of fibroblast growth factor-21 (FGF21) start increasing in patients with chronic kidney disease (CKD) since early stages during the cause of disease progression. FGF21 is a liver-derived hormone that induces responses to stress through acting on hypothalamus to activate the sympathetic nervous system and the hypothalamus-pituitary-adrenal endocrine axis. However, roles that FGF21 plays in pathophysiology of CKD remains elusive. Here we show in mice that FGF21 is required to survive CKD but responsible for blood pressure dysregulation. When introduced with CKD, Fgf21−/− mice died earlier than wild-type mice. Paradoxically, these Fgf21−/− CKD mice escaped several complications observed in wild-type mice, including augmentation of blood pressure elevating response and activation of the sympathetic nervous system during physical activity and increase in serum noradrenalin and corticosterone levels. Supplementation of FGF21 by administration of an FGF21-expressing adeno-associated virus vector recapitulated these complications in wild-type mice and restored the survival period in Fgf21−/− CKD mice. In CKD patients, high serum FGF21 levels are independently associated with decreased baroreceptor sensitivity. Thus, increased FGF21 in CKD can be viewed as a survival response at the sacrifice of blood pressure homeostasis.

Contribution of insulin resistance to decreased baroreceptor sensitivity & cardiometabolic risks in pre-obesity & obesity.

Background & objectives:Although insulin resistance (IR) is a known complication in obesity, the physiological mechanisms linking IR with cardiometabolic risks in obesity have not been well studied. This study was conducted to assess the difference in cardiovascular (CV) risk profile in IR and non-IR (NIR) conditions, and contribution of IR to cardiometabolic risks in pre-obese and obese individuals.Methods:Basal CV, blood pressure variability, autonomic function test and cardiometabolic parameters were recorded in pre-obese (n=86) and obese (n=77) individuals during 2012 and 2015. The association of altered cardiometabolic parameters with homeostatic model for IR (HOMA-IR) in pre-obese and obese groups and with baroreceptor sensitivity (BRS) in IR and NIR groups was calculated by appropriate statistical analysis.Results:Decreased BRS, a known CV risk and cardiometabolic parameters were significant in IR (pre-obese and obese) group compared to the NIR group. Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activities was observed in individuals with IR. There was no significant difference in the level of independent contribution of HOMA-IR to cardiometabolic parameters in pre-obese and obese groups. Adiponectin and inflammatory markers had an independent contribution to BRS in IR group.Interpretation & conclusions:Findings of the present study demonstrated that the intensity of cardiometabolic derangements and CV risk were comparable between IR, pre-obese and obese individuals. Pro-inflammatory state, dyslipidaemia and hypoadiponectinaemia might contribute to CV risk in these individuals with IR. IR could possibly be the link between altered metabolic profile and increased CV risks in these individuals independent of the adiposity status.

Diabetic status and grade of nonalcoholic fatty liver disease are associated with lower baroreceptor sensitivity in patients with nonalcoholic fatty liver disease

Baroreceptor sensitivity (BRS), a functional consequence of vascular stiffness, may be affected by the presence of diabetes mellitus (DM) and nonalcoholic fatty liver disease (NAFLD). The present study was designed to assess the effect of diabetic status and NAFLD grade on the BRS in patients with NAFLD. Seventy-five individuals (25 NAFLD without DM, 25 NAFLD with DM and 25 controls) were recruited for the study who underwent anthropometric and body composition analysis along with estimation of plasma glucose, serum insulin and serum lipids. BRS and blood pressure variability (BPV) analysis was carried out in both time and frequency domains. Carotid-radial and carotid-dorsalis pedis artery pulse wave velocity, and radial artery augmentation index were computed as measures of arterial stiffness. BRS was found to be lower in the NAFLD with DM group as well those with grade II NAFLD compared with the controls. Correlation analysis showed a negative correlation of BRS with postprandial blood glucose level (r=-0.39) and BMI (r=-0.467). The diabetic status and grade of NAFLD were associated independently with a decrease in BRS as well as the low-frequency component of diastolic BPV. The augmentation index and carotid-distal pulse wave velocity were higher in the NAFLD with DM group compared with controls. Both the diabetic status and grade of NAFLD were shown to have an independent effect on the decrease in the BRS with a consequent effect on BPV, with a greater influence of diabetic status rather than NAFLD grade on arterial stiffness.

Effect of Superficial Cervical Plexus Block on Baroreceptor Sensitivity in Patients Undergoing Carotid Endarterectomy

Regional anesthesia for patients undergoing carotid endarterectomy is associated with improved intraoperative hemodynamic stability compared with general anesthesia. The authors hypothesized that the reported advantages might be related to attenuated ipsilateral baroreflex control of blood pressure, caused by chemical denervation of the carotid bulb baroreceptor nerve fibers. A prospective cohort study. Single-center university hospital. The study included 46 patients undergoing carotid endarterectomy using superficial cervical block. A noninvasive computational periprocedural measurement of baroreceptor sensitivity was performed in all patients. Two groups were formed, depending on the patients' subjective response to surgical stimulation regarding the necessity of additional intraoperative local anesthesia (LA) administration on the carotid bulb. Group A (block alone) included 23 patients who required no additional anesthesia, and group B (block + LA) consisted of 23 patients who required additional anesthesia. Baroreceptor sensitivity showed no significant change after application of the block in both groups (group A: median [IQR], 5.19 [3.07-8.54] v 4.96 [3.1-9.07]; p = 0.20) (group B: median [IQR], 4.47 [3.36-8.09] v 4.53 [3.29-8.01]; p = 0.55). There was a significant decrease in baroreceptor sensitivity in group B after intraoperative LA administration (median [IQR], 4.53 [3.29-8.01] v 3.31 [2.26-7.31]; p = 0.04). Standard superficial cervical plexus block did not impair local baroreceptor function, and, therefore, it was not related to improved cerebral perfusion in awake patients undergoing carotid endarterectomy. However, direct infiltration of the carotid bulb was associated with the expected attenuation of baroreflex sensitivity.

Diurnal Blood Pressure Pattern in Patients with Ischemic and Dilated Cardiomyopathy

PP-057 Heart failure is a chronic progression characterized by neuroendocrine system maladaptation. This chronic progressive situation reflects an increase in sympathetic activity and peripheral vascular resistance and a decrease in baroreceptor sensitivity, and could be the cause of changes in the

Abstract 085: Anti-Inflammatory Treatment Reverses The Age-Related Increase In Catecholamine Biosynthetic Enzyme Tyrosine Hydroxylase And NYP In The Adrenal Medulla

Aging is associated with both elevated blood pressure and decreased baroreceptor sensitivity. These have been attributed to increased sympathetic nerve activity with age. One marker of sympathoactivation is protein levels of tyrosine hydoxylase (TH) in the adrenal medulla (AM), and TH levels markedly increase with age. There is also an increase in inflammation with age. To test the hypothesis that increased inflammation with age contributes to the elevated TH levels in the AM, we examined treatment with the anti-inflammatory agents, indomethacin (10 mg/kg, BID) or rosiglitazone (1 mg/kg, BID) on TH synthesis in F344 rats of three ages, 5, 12, 18 months. In addition, NPY, a peptide that is synthesized and co-released with catecholamines in the AM, as well as angiotensin II receptor subtypes, AT1 and AT2 protein levels were assessed in the AM following the anti-inflammatory treatments. Indomethacin and rosiglitazone were administered orally as part of a frozen strawberry treat for 16 days. Although there were no changes in TH or NPY levels between the 5 mo and 12 mo old control animals, TH and NPY were elevated by 27% and 45% (P&lt;0.05), respectively in the 18 compared with 5 mo rats. These age-related increases were completely reversed by treatment with indomethacin or rosiglitazone (P&lt;0.05). There was no effect of either treatment on AT1 or AT2 receptor protein, although AT1 receptor protein levels diminished slightly with age. These data indicate that anti-inflammatory treatment reverses the elevated TH and NPY in AM with age. Increased inflammation with age indirectly through elevated catecholamine synthesis may be contributing to the increased prevalence of hypertension with age.

Blood pressure and age associated with silent autonomic dysreflexia during urodynamic examinations in patients with spinal cord injury

An observational study. To investigate the factors associated with silent autonomic dysreflexia (AD) during urodynamics (UD) in spinal cord injury (SCI) patients. Taichung city, Taiwan, ROC. Blood pressure (BP) and symptoms of AD were continuously monitored during UD, and systolic blood pressure (SBP) elevations >20 mmHg was considered an AD reaction. AD patients were divided into a symptomatic group and a silent group (without AD symptoms), and variables (basic demographic data, hemodynamic data and UD parameters) were compared. A total of 42 patients, 21 in symptomatic and 21 in silent AD groups, were analyzed. Symptomatic group had significantly greater diastolic blood pressure (DBP) increment and rates of SBP/DBP changes (change of BP divided by duration) as compared to the silent group (29.5 vs 21.7 mmHg; 4.8 vs 2.3 mmHg min(-1) and 2.8 vs 1.4 mmHg min(-1)) (P<0.05). The cutoff points of these three variables, determined by receiver operating characteristic analysis, are: DBP increment of 21 mmHg and rates of SBP/DBP change of 2.27 and 1.16 mmHg min(-1). Age had a weak negative correlation with DBP change (Pearson's r=-0.377, P=0.048) and the silent group was significantly older than the symptomatic group (49.4 vs 40.1 years, P<0.05). Patients with more symptomatic AD tended to have significant DBP elevation and more rapid SBP/DBP increments, and this was negatively correlated with age. Aging decreases AD symptoms and the magnitude of DBP elevation, possibly through the mechanism of decreased baroreceptor sensitivity. BP monitoring during UD and other invasive procedures is strongly recommended, especially for elderly SCI patients.

Hemodynamic Changes after Eversion Carotid Endarterectomy: A Reason for Concern?

Hemodynamic Changes after Eversion Carotid Endarterectomy: A Reason for Concern?

Eversion Carotid Endarterectomy is Associated with Decreased Baroreceptor Sensitivity Compared to the Conventional Technique

ObjectiveImpairment of baroreceptor sensitivity (BRS) has been shown to be associated with blood pressure instability after carotid endarterectomy (CEA). The aim of this study was to determine whether there is a difference in postoperative BRS changes following eversion CEA (E-CEA) and conventional CEA (C-CEA). MethodsSixty-four patients undergoing E-CEA (n = 37) and C-CEA (n = 27) were prospectively studied. Non-invasive measurements of mean arterial pressure (MAP), cardiac output (CO) and total peripheral resistance (TPR) were perioperatively obtained over three 10-min periods. Baroreflex gain was calculated as the sequential cross-correlation between heart rate and beat-to-beat systolic blood pressure. ResultsCompared with changes observed after C-CEA, E-CEA was associated with an increase in systolic pressure (SP) (P = 0.01), diastolic pressure (DP) (P = 0.008), MAP (P = 0.002) and heart rate (HR) (P = 0.03) on postoperative day 1 (POD-1). BRS decreased after E-CEA from 6.33 to 4.71 ms mmHg−1 on POD-1 (P = 0.001) and to 5.26 ms mmHg−1 on POD-3 (P = 0.0004). By contrast, BRS increased after C-CEA from 4.59 to 6.13 ms mmHg−1 on POD-1 (P = 0.002) and to 6.27 ms mmHg−1 on POD-3 (P < 0.0001). ConclusionE-CEA and C-CEA have different effects on BRS. This is associated with an altered haemodynamic behaviour after E-CEA and C-CEA, respectively. These findings are likely the result of carotid sinus nerve interruption during E-CEA and preservation with C-CEA.

Twenty-four-Hour Ambulatory Blood Pressure Monitor Heart Rate: A Potential Marker for Gestational Hypertension in at-Risk Women

We prospectively correlated the 24-hour ambulatory blood pressure measurements (ABPM) to conventional sphygmomanometer blood pressure measurements (CSM) in women at risk for gestational hypertensive disorders (GHTNDs) and identified predictive factors from ABPM for GHTND. We analyzed 73 women with ≥ 1 risk factor for developing a GHTND. Using both the CSM and ABPM, the systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), and heart rate (HR) were measured for 24 hours during three periods (14 to 24 weeks; 24 to 32 weeks; and 33 weeks to delivery). Correlation between the CSM and ABPM lessened as pregnancy progressed. Seventeen (25%) of women developed a GHTND. MAP variability increased in the GHTND group versus those without a GHTND. The odds of developing a GHTND increased 1.5 times for every 1 beat per minute increase in the ABPM 24-hour HR at visit 1 and reversed by visit 3. In women at risk for a GHTND, CSM and ABPM correlate less well as pregnancy advances. HR changes in at-risk women may be a marker for the development of a GHTND and may reflect increased sympathetic activity and/or decreased baroreceptor sensitivity.

Cardiovascular Autonomic Modulation after Acute High Intensity Interval versus Aerobic Exercise

Little is known about autonomic modulation following high intensity interval exercise. PURPOSE: To compare cardiovascular autonomic modulations following acute high intensity interval versus endurance exercise. METHODS: Twenty five (∼25 y), endurance trained subjects completed a high intensity interval exercise session (IE) and an aerobic exercise session (AE) in randomized order on separate days. Beat-to-beat BP was recorded for 5 min in a supine position prior to exercise (PRE) and at 30 min (P30) and 60 min (P60) following exercise. Baroreceptor sensitivity (BRS) was analyzed by sequence (up-up and down-down) and spectral methods (transfer function, Alpha-high frequency and low frequency). Frequency domain of heart rate variability was derived from beat-to-beat BP data. Natural log-transformed heart rate high frequency (In HF) and low frequency (In LF) oscillations were calculated. Carotid BP was assessed using applanation tonometry at PRE, P30 and P60. RESULTS: Data presented in Table 1 as Mean (SE). The decrease in BRS and HRV post exercise was greater following IE than AE.TABLE 1: NO caption available.CONCLUSIONS: IE and AE elicit differential autonomic responses, demonstrated by lower parasympathetic modulation with altered BRS after interval exercise. These post-exercise responses may be related to an increase in carotid BP following IE. These data suggest that the vagal rebound during recovery from exercise is reduced or delayed following acute high intensity compared to acute endurance exercise.

Decreased mRNA expression of ASIC2a in nodose sensory ganglia is associated with development of hypertension in SHR

We recently demonstrated Acid-Sensing Ion Channel 2 (ASIC 2), a putative mechanosensitive ion channel subunit, expressed in somata in nodose sensory ganglia (NG) and terminals of the aortic depressor nerve in aortic arch (FASEB J, 20:, 2006). In the present study, we tested the hypothesis that ASIC2a expression in NG is decreased in association with development of hypertension (HT) in spontaneously hypertensive rats (SHR). Total RNA was obtained from both NG of SHR and normotensive WKY rats at 1, 3 and 16 months of age (n = 5–6 male rats at each age). HT develops between 1 and 3 months of age in SHR, ASIC2a mRNA expression measured by qPCR was stable in NG of WKY rats from 1 to 16 months (m) of age (Table). ASIC2a expression was increased in SHR vs. WKY NG at 1 month of age (pre-HT), but was markedly reduced in SHR NG at 3 and 16 months of age when SHR are HT (∗ p < 0.01). We conclude that ASIC2a expression in NG is markedly decreased in SHR in association with development of HT. The decreased expression cannot be attributed to nonspecific genetic differences in SHR vs. WKY since ASIC2a expression was increased in young pre-HT SHR-NG. We speculate that the reduction of ASIC2a expression may contribute to decreased baroreceptor sensitivity and HT in SHR (HL14388).

Stress – the Battle for Hearts and Minds: Links Between depression, Stress and Ischemic Heart Disease

Depression and ischemic heart disease (IHD) are strongly related common disorders. Depression itself is an independent cardiac risk factor and is associated with a two- to threefold increase in IHD mortality. Attention has now shifted to identifying the common underlying mechanisms that could make individuals susceptible to both disorders. Abnormalities that have been implicated in this relationship include abnormal platelet activation, decreased baroreceptor sensitivity and endothelial dysfunction. Depression and IHD both have a high association with environmental stress, and depression is characterized by abnormalities of the stress-hormone axis. This review provides a brief overview of some recent developments in our understanding of the pathophysiological links between stress, depression and IHD.

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

Heat stroke is characterized by hyperthermia, arterial hypotension, decreased baroreflex sensitivity, and increased serum levels of β-endorphin. Whereas naltrexone may have therapeutic potential in heat stroke, the underlying mechanism remains unclear. We tested the hypothesis that naltrexone may attenuate heat stroke by reducing hyperthermia, hypotension, decreased baroreceptor sensitivity, and/or increased serum levels of β-endorphin. Heat stroke was induced by exposing the anesthetized adult Sprague-Dawley rats in an incubator at 43°C. The moment in which the mean arterial pressure dropped irreversibly from the peak level was taken as the onset of heat stroke. Control rats were exposed to 24°C. Mean arterial pressure, baroreceptor sensitivity, and maximal reflex bradycardia, after the onset of heat stroke, were all significantly lower than in control rats. However, rectal temperature and serum levels of β-endorphin were all greater after the onset of heat stroke. Intravenous delivery of naltrexone (10 mg/kg) 20 min before the initiation of heat stress, but not immediately at the onset of heat stroke, significantly attenuated the above-mentioned reactions. Accordingly, naltrexone improved survival during heat stroke. These results suggest that naltrexone protects against hypotension and decrement of both baroreceptor sensitivity and maximal reflex bradycardia during heat stroke by reducing both hyperthermia and increment of serum β-endorphin and thus improves survival.

Stress, depression and cardiac arrhythmias

A relationship between behavioural factors and cardiac arrhythmogenesis in humans has been described. Three sets of conditions contribute to the occurrence of arrhythmias: myocardial electrical instability, most often due to coronary artery disease; an acute triggering event, frequently related to mental stress; and a chronic, pervasive, and intense psychological state, often including depression and hopelessness. The autonomic nervous system plays an important role in the occurrence of cardiac arrhythmias and it is well documented that mood alterations as mental stress and depression influence cardiac autonomic balance. There is an increasing body of evidence that patients with the greatest changes in cardiac neural regulation with decreased parasympathetic tone coupled with increased sympathetic activity are at the greatest risk for developing fatal ventricular arrhythmias. These patients have a reduced heart rate variability, increased QT-dispersion and a decreased baroreceptor sensitivity. The influence of stress and depression on the autonomic nervous system and the impact on the occurrence of both atrial and ventricular arrhythmias is being discussed.

Early autonomic malfunction in normotensive individuals with a genetic predisposition to essential hypertension.

One of the primary pathologies associated with hypertension is a complex autonomic dysfunction with evidence of sympathetic hyperactivity and/or vagal withdrawal. We investigated the possibility for early detection of essential hypertension on the basis of the analysis of heart rate (HR) and blood pressure fluctuations, which reflect autonomic control. Young adult normotensive offspring of one hypertensive parent (KHT; n = 12) and normotensive offspring of two normotensive parents (YN; n = 14) participated in this study. ECG, continuous blood pressure, and respiration were recorded during steady-state conditions and under various autonomic challenges. Time-frequency decomposition of these signals was performed with the use of a continuous wavelet transform. The use of the wavelet transform enables the extension of typical HR variability analysis to non-steady-state conditions. This time-dependent spectral analysis of HR allows time-dependent quantification of different spectral components reflecting the sympathetic and parasympathetic activity during rapid transitions, such as an active change in posture (CP). During an active CP from the supine to standing position, KHT demonstrated a significantly greater increase in the low-frequency fluctuations in HR than YN, indicating enhanced sympathetic involvement in the HR response to CP, and a reduced alpha-index, indicating decreased baroreceptor sensitivity. On recovery from handgrip, vagal reactivation was more sluggish in KHT. These results indicate the early existence of malfunctions in both branches of autonomic control in individuals at increased risk of hypertension.