Baroreflex

To reveal the functional importance of amino acid neurotransmission in the amygdala (AMY) of conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, the in vivo release of glutamate (GLU) and GABA in this brain structure was studied using the push-pull superfusion technique. Basal GLU and GABA release rates in the AMY were comparable in SHR and WKY rats, although arterial blood pressure (BP) in SHR (15266 mmHg) was higher than in WKY rats (10264 mmHg). Neuronal depolarization by superfusion with veratridine enhanced the release of GLU and GABA to a similar extent in both rat strains. On the other hand, exposure to noise stress (95 dB) for 3 min led to a tetrodotoxin-sensitive increase in GLU release in the AMY of SHR, but not WKY rats. The concurrent pressor response to noise was enhanced in SHR as compared to WKY rats. A rise in BP induced by intravenous infusion of phenylephrine for 9 min had no effect on amino acid release in the AMY of both strains. The data suggest an exaggerated stress response of glutamatergic neurons in the AMY of SHR as compared with WKY rats, which might be of significance for the strain differences in the cardiovascular and behavioural responses to stress. The results also show that, in both rat strains, glutamatergic and GABAergic neurons in the AMY are not modulated by baroreceptor activation. Moreover, hypertension in adult SHR does not seem to be linked to a disturbed synaptic regulation of glutamatergic or GABAergic transmission in the AMY.

We studied healthy supine astronauts on Earth with electrocardiogram, non-invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings. r The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs. r R-R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea. r The subjects' responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity.

Cirrhotic cardiomyopathy is a clinical syndrome in patients with liver cirrhosis characterized by an abnormal and blunted response to physiologic, pathologic, or pharmacologic stress but normal to increased cardiac output and contractility at rest. As many as 50% of cirrhotic patients undergoing liver transplantation show signs of cardiac dysfunction, and 7% to 21% of deaths after orthotopic liver transplantation result from overt heart failure. In this review, we critically evaluate the existing literature on the pathophysiology and clinical implications of cirrhotic cardiomyopathy. (J Am Coll Cardiol 2010;56:539-49)

The objective of the present study was to identify metabolic, cardiovascular and autonomic changes induced by fructose overload administered in the drinking water of rats for 8 weeks. Female Wistar rats (200-220 g) were divided into 2 groups: control (N = 8) and fructose-fed rats (N = 5; 100 mg/L fructose in drinking water for 8 weeks). The autonomic control of heart rate was evaluated by pharmacological blockade using atropine (3 mg/kg) and propranolol (4 mg/kg). The animals were submitted to an intravenous insulin tolerance test (ITT) and to blood glucose measurement. The fructose overload induced a significant increase in body weight (~10%) and in fasting glycemia (~28%). The rate constant of glucose disappearance (KITT) during ITT was lower in fructose-fed rats (3.25 ± 0.7%/min) compared with controls (4.95 ± 0.3%/min, P < 0.05) indicating insulin resistance. The fructose-fed group presented increased arterial pressure compared to controls (122 ± 3 vs 108 ± 1 mmHg, P < 0.05) and a reduction in vagal tonus (31 ± 9 vs 55 ± 5 bpm in controls, P < 0.05). No changes in sympathetic tonus were observed. A positive correlation, tested by the Pearson correlation, was demonstrable between cardiac vagal tonus and KITT (r = 0.8, P = 0.02). These data provided new information regarding the role of parasympathetic dysfunction associated with insulin resistance in the development of early metabolic and cardiovascular alterations induced by a high fructose diet.

This paper reviews the published work of me along with my students and close colleagues on the topic of heart rate variability biofeedback (HRVB). It includes early research by Vaschillo documenting resonance characteristics of the baroreflex system that causes large oscillations in heart rate when breathing at resonance frequency, research on heart rate variability as a marker of parasympathetic stress response in asthma, and HRVB as a treatment for asthma and depression. Many questions about HRVB remain unresolved, and important questions for future research are listed.

Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment ...

Sleep disordered breathing (SDB) ranges in severity from primary snoring (PS) to obstructive sleep apnoea (OSA). In adults, SDB is associated with adverse cardiovascular consequences which are mediated, in part, by autonomic dysfunction. Although SDB is common in children, fewer paediatric studies have investigated these cardiovascular effects. Initial research focused on those with OSA, indeed children with PS were occasionally utilised as the comparison control group. However, it is essential to understand the ramifications of this disorder in all its severities, as currently the milder forms of SDB are often untreated. Methodologies used to assess autonomic function in children with SDB include blood pressure (BP), BP variability, baroreflex sensitivity, heart rate variability, peripheral arterial tonometry and catecholamine assays. The aim of this review was to summarise the findings of paediatric studies to date and explore the relationship between autonomic dysfunction and SDB in children, paying particular attention to the roles of disease severity and/or age. This review found evidence of autonomic dysfunction in children with SDB during both wakefulness and sleep. BP dysregulation, elevated generalised sympathetic activity and impairment of autonomic reflexes occur in school-aged children and adolescents with SDB. The adverse effects of SDB seem somewhat less in young children, although more studies are needed. There is mounting evidence that the cardiovascular and autonomic consequences of SDB are not limited to those with OSA, but are also evident in children with PS. The severity of disease and age of onset of autonomic consequences may be important guides for the treatment of SDB.

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Space exploration is a dream of mankind. However, this intriguing environment is not without risks. Life, and the human body, has developed all over evolution in the constant presence of gravity, especially from the moment on when living creatures left the ocean. When this gravitational force is no longer acting on the body, drastic changes occur. Some of these changes occur immediately, others progress only slowly. In the past 40 years of human space flight (first orbital flight by Yuri Gagarin on 12 April, 1961) several hazards for the human body have been identified. Bone mineral density is lost, muscle atrophy and cardiovascular deconditioning occur, pulmonary function, fluid regulating systems of the body, sensory and the balance system are all disturbed by the lack of gravity. These changes in human physiology have to be reversed again when astronauts return to Earth. This can cause adaptation problems, especially after long-duration space flights. Also the reaction of human physiology to radiation in space poses a huge risk at this moment. In this review the accent will be on cardiovascular function in space: how normal function is modified to reach a new equilibrium in space after short and long duration exposure to microgravity. In order to make long-duration space flight possible the mechanisms of this physiological adaptation must be understood to full extend. Only with this knowledge, effective countermeasures can be developed.

Aging and obesity both have a significant impact on central blood pressure (BP) regulation, and previous studies indicated that changes in central redox signaling with age may affect high-fat (HF) diet-induced cardiovascular responses. Therefore, we investigated the effects of 60% HF feeding on BP regulation in young adult (5 mo) and old (26 mo) Fischer-344 × Brown-Norway rats. Radiotelemetric transmitters were implanted to measure BP, heart rate (HR), locomotor activity, and spontaneous baroreflex sensitivity. Expression and activity of NADPH oxidase and ANG II type 1 receptor were assessed in the hypothalamus and in the nucleus tractus solitarii. Old animals gained more weight on HF diet compared with young, whereas central NADPH oxidase expression and activity elevated similarly in the two age groups. After an initial hypotensive and tachycardic response during the first week of HF feeding, BP in young animals increased and became significantly elevated after 6 wk of HF feeding. ...

Slow, deep, pranayama-based breathing training has been shown to be effective in reducing blood pressure (BP). The present study was undertaken to determine immediate effects of performing pranava pranayama on cardiovascular parameters in hypertensive patients. 29 hypertensive patients who were on medical treatment and also attending yoga sessions were recruited for the present study. Supine heart rate (HR) and BP were recorded before and after performance of pranava pranayama for five minutes. Post intervention statistical analysis revealed a significant (P &lt; 0.05) reduction in systolic pressure (SP) and a more significant (P &lt; 0.01) reduction in HR, pulse pressure and double product (Do P). The reduction in rate-pressure product (RPP) was highly significant (P &lt; 0.001). Pranava pranayama is effective in reducing HR and SP in hypertensive patients within five minutes of the practice. This may be due to a normalization of autonomic cardiovascular rhythms as a result of incr...

Recent studies suggest that ruminative thoughts may be mediators of the prolonged physiological effects of stress. We hypothesized that autonomic dysregulation plays a role in the relation between rumination and health. Rumination was induced by an anger-recall task in 45 healthy subjects. Heart rate variability (HRV), baroreflex sensitivity (BRS), and baroreflex effectiveness index (BEI) change scores were evaluated to obtain the autonomic phenotype of rumination. Personality traits and endothelial activation were examined for their relation to autonomic responses during rumination. Degree of endothelial activation was assessed by circulating soluble intercellular adhesion molecule-1 (sICAM-1). Vagal withdrawal during rumination was greater for women than men. Larger decreases in the high frequency component of HRV were associated with higher levels of anger-in, depression, and sICAM-1 levels. BRS reactivity was negatively related to trait anxiety. BEI reactivity was positively related to anger-in, hostility, anxiety, and depression. Lower BEI and BRS recovery were associated with lower social desirability and higher anger-out, anxiety, and depression. Findings suggest that the autonomic dysregulation that characterizes rumination plays a role in the relationships between personality and cardiovascular health.

objective of this study is to develop a model of the cardiovascular system capable of simulating the short-term (Յ5 min) transient and steady-state hemodynamic responses to head-up tilt and lower body negative pressure. The model consists of a closedloop lumped-parameter representation of the circulation connected to set-point models of the arterial and cardiopulmonary baroreflexes. Model parameters are largely based on literature values. Model verification was performed by comparing the simulation output under baseline conditions and at different levels of orthostatic stress to sets of populationaveraged hemodynamic data reported in the literature. On the basis of experimental evidence, we adjusted some model parameters to simulate experimental data. Orthostatic stress simulations are not statistically different from experimental data (two-sided test of significance with Bonferroni adjustment for multiple comparisons). Transient response characteristics of heart rate to tilt also compare well with reported data. A case study is presented on how the model is intended to be used in the future to investigate the effects of postspaceflight orthostatic intolerance. mathematical model; simulation; head-up tilt; lower body negative pressure; orthostatic intolerance A MAJOR CARDIOVASCULAR PROBLEM in the present lifescience space program is orthostatic intolerance (OI) seen in astronauts on their return to the normal gravitational environment (16). Many hypotheses concerning the mechanisms leading to OI have been the focus of in-flight and ground-based experimental studies in the past, and some are presently under investigation in both human and animal studies (see ). Despite considerable efforts, there remains a lack of universal consensus about the fundamental etiology of postflight OI. To quantitatively supplement some of these studies, we have developed a computational model capable of simulating the short-term (Յ5 min) response of the cardiovascular system to gravitational challenge in normal and microgravity-adapted individuals.

Aim: To analyze the correlation of the Poincaré plot descriptors of RR intervals with standard measures of heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS). A physiological model of changing respiratory rates from 6 to 15 breaths/min provided a wide range of RR intervals for analysis. Material and methods: Beat-to-beat finger blood pressure, ECG, and respiratory curves were recorded noninvasively in 15 young healthy volunteers (19-25 years old; 7 females) breathing for 5 min at 4 different respiratory rates of 6, 9, 12, and 15 breaths/ min. Four descriptors of the Poincaré plot (SD1, SD2, S, and SD2/SD1), time and frequency domain HRV, and spontaneous BRS (cross-correlation method) were calculated for each 5-min recording. Results: The values of SD1 characterizing short-term HRV, SD2 describing long-term HRV, and S measuring total HRV were significantly correlated with BRS and time and frequency domain measures of short, long, and total HRV. The LF/ HF significantly correlated with SD2 and SD2/SD1 representing the balance between long-and short-term HRV. None of the Poincaré plot descriptors was correlated with the mean RR interval. The increased respiratory rate caused a significant reduction of BRS, measures of total and long-term HRV, and an increase of HF that peaked at 12 breaths/min. Conclusions: The descriptors of the Poincaré plot of RR intervals are significantly correlated with measures of BRS and time and frequency domain HRV, but not with heart rate. A faster respiratory rate reduces long-term HRV measures and temporarily increases HF.

The physiologic activity and mechanism of action of NO ؊ in vivo remains unknown. The NO ؊ generator Angeli's salt (AS, Na2N2O3) was administered to conscious chronically instrumented dogs, and pressure-dimension analysis was used to discriminate contractile from peripheral vascular responses. AS rapidly enhanced left ventricular contractility and concomitantly lowered cardiac preload volume and diastolic pressure (venodilation) without a change in arterial resistance. There were no associated changes in arterial or venous plasma cGMP. The inotropic response was similar despite reflex blockade with hexamethonium or volume reexpansion, indicating its independence from baroreflex stimulation. However, reflex activation did play a major role in the selective venodilation observed under basal conditions. These data contrasted with the pure NO donor diethylamine͞NO, which induced a negligible inotropic response and a more balanced veno͞arterial dilation. AS-induced positive inotropy, but not systemic vasodilatation, was highly redox-sensitive, being virtually inhibited by coinfusion of N-acetyl-L-cysteine. Cardiac inotropic signaling by NO ؊ was mediated by calcitonin gene-related peptide (CGRP), as treatment with the selective CGRP-receptor antagonist CGRP-(8 -37) prevented this effect but not systemic vasodilation. Thus, NO ؊ is a redox-sensitive positive inotrope with selective venodilator action, whose cardiac effects are mediated by CGRP-receptor stimulation. This fact is evidence linking NO ؊ to redox-sensitive cardiac contractile modulation by nonadrenergic͞noncholinergic peptide signaling. Given its cardiac and vascular properties, NO ؊ may prove useful for the treatment of cardiovascular diseases characterized by cardiac depression and elevated venous filling pressures.

The present study was done to determine if estrogen interacts with excitatory and / or inhibitory amino acid neurotransmitters to alter neuronal excitability within the parabrachial nucleus (PBN) and modulate autonomic tone. First, the role of estrogen in modulating autonomic tone was investigated in male rats anesthetized with Inactin (100 mg / kg). Animals were instrumented to record blood pressure, heart rate, vagal parasympathetic and renal sympathetic nerve activities as well as baroreflex sensitivity. Direct, bilateral injection of 17b-estradiol (0.5 mM; 200 nl / side) into the PBN resulted in a significant decrease in blood pressure (1764 mmHg), sympathetic tone (2065%) and heart rate (2265 beats / min) while increasing parasympathetic tone (3464%) 30 min post-injection. These estrogeninduced effects were completely blocked by the co-injection of estrogen with the estrogen receptor antagonist, ICI 182,780 (20 mM; 200 nl / side). Co-injection of the NMDA receptor antagonist, (6)-3-(2-carboxypiperazine-4-yl) propyl-1-phosphonic acid (CPP; 10 mM; 200 nl / side), with estradiol resulted in complete blockade of the estrogen-induced decrease in heart rate and increase in parasympathetic tone only. Co-injection of estradiol with the GABA receptor antagonist, (1)-bicuculline (0.1 mM; 200 nl / side), resulted in complete blockade A of the estrogen-induced decrease in blood pressure and sympathetic nerve activity only. These results suggest that estrogen acts on estrogen receptors on neurons in the PBN to modulate GABA -receptor mediated inhibitory neurotransmission to alter sympathetic tone A and blood pressure and on neurons in a separate, parallel pathway to modulate NMDA-receptor mediated neurotransmission to alter parasympathetic tone and heart rate. 

933 Heart Rate Variability in Sleep Related Alveolar Hypoventilation-Palma et al Sleep related alveolar hypoventilation (SRAH) is characterized by decreased alveolar ventilation resulting in sleep related oxygen arterial desaturation in patients with normal mechanical properties of the lung. SRAH can be distinguished from central and obstructive sleep apnea (OSA) by the fact that OSA is defined by periodic alterations in the respiratory flow (i.e., apnea, hypopnea, or respiratory effort-related arousals [RERAs]) that are not typically present in SRAH, even though both conditions (sleep apnea and SRAH) may coexist. In the absence of pulmonary parenchymal or vascular pathology, lower airway obstruction, neuromuscular disorders, or kyphoscoliosis, the disorder is referred to as idiopathic SRAH. When severe obesity is present, it predisposes individuals to developing SRAH by increasing the burden on disadvantaged respiratory muscles, and then the disorder can be referred to as obesity-related sleep hypoventilation syndrome, and is usually included in the spectrum of obesity-related hypoventilation

We evaluated the effect of exercise-induced hyperthermia (EIH) on autonomic nervous system (ANS) function in the early ( \( \dot{Q} \) ) were evaluated during the last min prior to a change in posture. Responses to 70° HUT were compared to the same challenge performed without prior exercise and under a NHS condition. Relative to NHS, \( \dot{Q} \) was maintained during the repeated HUT’s following EIH, despite significant reductions in SV and sustained elevations in esophageal temperature (p  \( \dot{Q} \) appears to be due to increased HR (HUT1: NRS = 76 ± 3 beats min−1, EIH = 126 ± 6 beats min−1) stemming from modulation of the ANS toward sympathetic dominance. Parasympathetic withdrawal was evidenced by a reduction in root mean squared successive difference (i.e., HUT1: NHS = 66 ± 12 ms, EIH = 9 ± 1 ms) of heart rate variability and paralleled by a reduction in baroreceptor sensitivity for all HUT’s following EIH (p Q is maintained and participants do not become orthostatic intolerant/syncopal during the short-term recovery period following EIH. Normal ANS and cardiovascular function is restored following 24 h of recovery.

The baroreceptor reflex is poorly known by most physicians even though is fundamental in stabilizing the blood pressure on a beat to beat basis and is crucial for survival. Its fascinating history is briefly reviewed in this article. In 1852 Claude Bernard discovered that the sympathetic nerves of the neck innervate the blood vessels of the skin of the rabbit. Edgar Douglas Adrian in 1932 demonstrated that the sympathetic nerves that innervate the blood vessels discharge spontaneously at a rate of 4-6 per second and thus discovered the physiological basis of the vasomotor tone. In the XIX century Ludwig Traube and Karl Constantine Ewald Hering discovered that blood pressure fluctuates synchronously with respiratory movements and Sigmund Mayer observed that there are also slow non respiratory fluctuations of blood pressure. In 1921 Heinrich Ewald Hering found that high pressure baroreceptors are located in the carotid sinuses and demonstrated that the stimulation of the afferent nerv...

We evaluated heart rate variability biofeedback as a method for increasing vagal baroreflex gain and improving pulmonary function among 54 healthy adults. Methods: We compared 10 sessions of biofeedback training with an uninstructed control. Cognitive and physiological effects were measured in four of the sessions. Results: We found acute increases in low-frequency and total spectrum heart rate variability, and in vagal baroreflex gain, correlated with slow breathing during biofeedback periods. Increased baseline baroreflex gain also occurred across sessions in the biofeedback group, independent of respiratory changes, and peak expiratory flow increased in this group, independently of cardiovascular changes. Biofeedback was accompanied by fewer adverse relaxation side effects than the control condition. Conclusions: Heart rate variability biofeedback had strong long-term influences on resting baroreflex gain and pulmonary function. It should be examined as a method for treating cardiovascular and pulmonary diseases. Also, this study demonstrates neuroplasticity of the baroreflex. Key words: biofeedback, heart rate variability, baroreflex, pulmonary function, neuroplasticity.

We were interested in a therapeutic device designed to increase carotid–cardiac baroreflex sensitivity (BRS) since high BRS is associated with a lower risk for development of hypotension in humans with experimentally–induced central hypovolemia. We hypothesized that spontaneous breathing through an impedance threshold device (ITD) designed to increase negative intrathoracic pressure during inspiration and elevate arterial blood pressure would acutely increase BRS in humans.We tested this hypothesis by measuring heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures, and carotid-cardiac BRS in 10 female and 10 male subjects breathing through a face mask at three separate ITD conditions: (a) 6 cm H2O; (b) 12 cm H2O; and (c) a control (0 cm H2O). HR was increased (P = 0. 013) from 64 ± 3 bpm during control to 68 ± 3 bpm at 6 cm H2O ITD and 71 ± 4 bpm at 12 cm H2O ITD breathing conditions. During ITD breathing, BRS was not altered but responses were shifted to higher arterial pressures. However, SBP and DBP were elevated for both the 6 and 12 cm H2O conditions compared to the 0 cm H2O condition, but returned to control (sham) levels by 30 minutes after cessation of ITD breathing. There were no gender effects for BRS or any hemodynamic responses to breathing through the ITD. We conclude that breathing with inspiratory impedance at relatively low pressures can increase baseline arterial blood pressure, i. e., reset the operational point for SBP on the baroreflex stimulus–response relationship, in healthy subjects. This resetting of the cardiac baroreflex may represent a mechanism that allows blood pressure to increase without a reflex–mediated reduction in HR.

In a previous study, we recorded short-term cardiovascular responses after a steep increase in arterial pressure in healthy humans [Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H199-H211, 1994]. The aim of the present study was to develop a mathematical model of the baroreflex control of arterial pressure, to use this model with the previously recorded data to estimate unknown parameters in the reflex control loop, and then to analyze the overall open- and closed-loop performance of the system by model simulations with use of individual sets of optimal parameters. The mathematical model consists of a heart, a linear elastic arterial reservoir, and two parallel resistive vascular beds. The arterial baroreflex loop is modeled by two separate time domain processing objects, each with its own gain, time constant, and delay, to simulate the action of a sympathetic signal to the peripheral vascular bed and a parasympathetic signal to the heart. In repeated model simulations, the control...

Trbovic, Sinisa M., Miodrag Radulovacki, and David W. Carley. Protoveratrines A and B increase sleep apnea index in Sprague-Dawley rats. J. Appl. Physiol. 83(5): 1602–1606, 1997.—The action of protovertarines A and B, which stimulate carotid sinus baroreceptors and vagal sensory endings in the heart as well as pulmonary bed, were assessed on spontaneous and postsigh central sleep apneas in freely moving Sprague-Dawley rats. During the 6-h recording period, animals were simultaneously monitored for sleep by using electroencephalogram and electromyogram recordings, for respiration by single-chamber plethysmography, and for blood pressure and heart period by using radiotelemetry. After administration of 0.2, 0.5, or 1 mg/kg sc of protoveratrines, cardiopulmonary changes lasting at least 6 h were observed in all three behavioral states [heart period increased up to 23% in wakefulness, 21% in non-rapid-eye-movement (non-REM) sleep, and 20% in REM sleep; P &lt; 0.005 for each]. At the sam...

The analysis of blood pressure (BP) and heart rate (HR) variability is currently used to investigate the mechanisms responsible for cardiovascular control; therefore, we assessed whether an impairment of 24-h BP and HR profiles and sympathovagal interaction modulating cardiovascular function was present in patients with thalassemia major (TM) in preclinical phase of heart disease. Nine beta-thalassemic patients 18 years old without clinical signs of cardiac failure and 9 age- and sex-matched controls were studied. Twenty-four-hour-ambulatory BP and HR were measured using the SpaceLabs 90207 device. A truncated Fourier series with four harmonics was used to describe the diurnal blood pressure profile. Mean 24-h ambulatory systolic BP, diastolic BP, and mean arterial pressure were significantly lower in TM patients than in normal subjects (P &lt; .05). A significantly higher nighttime HR value was found in TM patients (P &lt; .05). More than 40% of the TM patients did not show a signi...

Cardiovascular diseases are the most frequent causes of morbidity and mortality around the world. However, during last decades, an improvement was made in diagnosis and therapy of cardiovascular diseases, there was still a need for better understanding of their pathophysiology. Among neurohormonal systems, SNS plays a central role in cardiovascular regulation in both health and disease. Involvement of SNS in pathogenesis of hypertension, coronary artery disease or heart failure is well known and proved. Methods such as microneurography, direct catecholamine measurements, heart rate variability or baroreflex sensitivity assessment allowed studying sympathetic activity and its influence on cardiovascular disorders. Although introduced into scientific practice methods of SNS evaluation are not commonly used in the clinic. However, two of the methods: analysis of heart rate variability (HRV) and baroreflex sensitivity (BRS) were recommended as the diagnostic tools and can be found in cl...

Aim: 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 the heart rate variability (HRV) and BRS following 4 weeks of resistance or aerobic training in a population with borderline high blood pressure (BP). Methods: Twenty-nine mild hypertensives were recruited and randomly assigned to 4 weeks of RE or AE training. Before and after training, resting measures of HRV frequencies and BRS were obtained. Results: There was a significant decrease in resting systolic BP for both exercise training modes (RE 136 AE 3.0 pre-to 132 AE 3.4 post-training vs. AE 142 AE 4.0 pre-to 137 AE 3.6 mmHg post-training, P = 0.019). Diastolic BP decreased significantly following both exercise training modes (RE 78 AE 1.31 pre to 74 AE 1.1 post vs. AE 80 AE 1.7 pre to 77 AE 1.6 mmHg post, P = 0.002). A significant time by training mode interaction for low frequency : high frequency (HF) ratio (P = 0.017) with AE decreasing the ratio (275.21 AE 67.28 to 161.26 AE 61.49) and RE increasing this ratio (143.73 AE 65.00 to 227.83 AE 59.41). Natural log-transformed (ln) HRV values showed a timeby-training mode interaction for ln HF (P = 0.05) as ln HF increased (4.7 AE 0.38 to 5.4 AE 0.35 ms 2 ) following AE and decreased (5.98 AE 0.37 to 5.76 AE 0.42 ms 2 ) following RE. BRS increased following aerobic training and decreased after resistance training (6.74 AE 1.2 to 7.94 AE 1.3 and 10.44 AE 1.2 to 9.1 AE 1.2 ms mmHg )1 respectively, P = 0.021). Conclusions: Aerobic exercise improved the autonomic nervous system (increasing vagal tone, reducing sympathovagal balance while increasing BRS) while RE showed no improvements in cardiac autonomic tone and decreased BRS.

The statistical association between endurance exercise capacity and cardiovascular disease suggests that impaired aerobic metabolism underlies the cardiovascular disease risk in men and women. To explore this connection, we applied divergent artificial selection in rats to develop low-capacity runner (LCR) and high-capacity runner (HCR) rats and found that disease risks segregated strongly with low running capacity. Here, we tested if inborn low aerobic capacity promotes differential sex-related cardiovascular effects. Compared with HCR males (HCR-M), LCR males (LCR-M) were overweight by 34% and had heavier retroperitoneal, epididymal, and omental fat pads; LCR females (LCR-F) were 20% heavier than HCR females (HCR-F), and their retroperitoneal, but not perireproductive or omental, fat pads were heavier as well. Unlike HCR-M, blood pressure was elevated in LCR-M, and this was accompanied by left ventricular (LV) hypertrophy. Like HCR-F, LCR-F exhibited normal blood pressure and LV w...

Heart rate and blood pressure, as well as other physiological systems, among healthy people, show a complex pattern of variability, characterized by multifrequency oscillations. There is evidence that these oscillations reflect the activity of homeostatic reflexes. Biofeedback training to increase the amplitude of respiratory sinus arrhythmia (RSA) maximally increases the amplitude of heart rate oscillations only at approximately 0.1 Hz. To perform this task people slow their breathing to this rate to a point where resonance occurs between respiratory-induced oscillations (RSA) and oscillations that naturally occur at this rate, probably triggered in part by baroreflex activity. We hypothesize that this type of biofeedback exercises the baroreflexes, and renders them more efficient. A manual is presented for carrying out this method. Supporting data are provided in Lehrer, Smetankin, and Potapova (2000) in this issue.

This study describes the use of a biofeedback method for the noninvasive study of baroreflex mechanisms. Five previously untrained healthy male participants learned to control oscillations in heart rate using biofeedback training to modify their heart rate variability at specific frequencies. They were instructed to match computer-generated sinusoidal oscillations with oscillations in heart rate at seven frequencies within the range of 0.01-0.14 Hz. All participants successfully produced high-amplitude target-frequency oscillations in both heart rate and blood pressure. Stable and predictable transfer functions between heart rate and blood pressure were obtained in all participants. The highest oscillation amplitudes were produced in the range of 0.055-0.11 Hz for heart rate and 0.02-0.055 Hz for blood pressure. Transfer functions were calculated among sinusoidal oscillations in the target stimuli, heart rate, blood pressure, and respiration for frequencies at which subjects receive...

We examined (a) whether carotid baroreceptor stimulation attenuates the auditory startle response and its modulation by preceding affective pictures, and (b) whether these effects are mediated by endogenous opioids. Seventy-eight young normotensive adults with or without a parental history of hypertension received brief exposures to affective pictures and noise bursts during phasic manipulation of the carotid baroreceptors. In each participant, opioids were blocked by naltrexone in half of the sessions. Baroreceptor stimulation had a strong dampening effect on the startle response. This effect was not influenced by opioid blockade, sex, or parental history of hypertension. No baroreceptor effects were obtained regarding ratings of the affective pictures or startle modulation by the pictures. The baroreceptor stimulation effects seem to be mediated by the basal primary acoustic startle circuit rather than by higher affective circuits.

A systematic discussion on linear as well as non-linear compartmental models of the cardiovascular system and its various feedback mechanism is given. Most of the results are independent of explicit functional expressions. The topological structure of the model is essential for the response to a local change in peripheral resistance. Inclusion of Parallel paths versus serial paths gives qualitatively different response. Global asymptotic stability follows from the general theory.