Showing papers on "Autonomic nervous system published in 2001"

Role of endogenous opioid system in the regulation of the stress response.

Abstract: Numerous studies and reviews support an important contribution of endogenous opioid peptide systems in the mediation, modulation, and regulation of stress responses including endocrine (hypothalamopituitary-adrenal, HPA axis), autonomic nervous system (ANS axis), and behavioral responses. Although several discrepancies exist, the most consistent finding among such studies using different species and stressors is that opioids not only diminish stress-induced neuroendocrine and autonomic responses, but also stimulate these effector systems in the non-stressed state. A distinctive feature of the analgesic action of opioids is the blunting of the distressing, affective component of pain without dulling the sensation itself. Therefore, opioid peptides may diminish the impact of stress by attenuating an array of physiologic responses including emotional and affective states. The widespread distribution of enkephalin (ENK) throughout the limbic system (including the extended amygdala, cingulate cortex, entorhinal cortex, septum, hippocampus, and the hypothalamus) is consistent with a direct role in the modulation the stress responses. The predictability of stressful events reduces the impact of a wide range of stressors and ENK appears to play an important role in this process. Therefore, ENK and its receptors could represent a major modulatory system in the adaptation of an organism to stress, balancing the response that the stressor places on the central stress system with the potentially detrimental effects that a sustained stress may produce. Chronic neurogenic stressors will induce changes in specific components of the stress-induced ENKergic system, including ENK, delta- and mu-opioid receptors. This review presents evidences for adaptive cellular mechanisms underlying the response of the central stress system when assaulted by repeated psychogenic stress, and the involvement of ENK in these processes.

Parasympathetic and sympathetic control of the pancreas: A role for the suprachiasmatic nucleus and other hypothalamic centers that are involved in the regulation of food intake

Abstract: To reveal brain regions and transmitter systems involved in control of pancreatic hormone secretion, specific vagal and sympathetic denervation were combined with injection of a retrograde transsynaptic tracer, pseudorabies virus (PRV), into the pancreas After sympathetic or vagal transsection first-order neurons were revealed in the dorsal motor nucleus of the vagus (DMV) or in preganglionic spinal cord neurons (SPN), respectively Careful timing of the survival of the animals allowed the detection of cell groups in immediate control of these DMV or SPN neurons A far larger number of cell groups is involved in the control of DMV than of SPN neurons Examples are given of a high level of interaction between the sympathetic and parasympathetic nervous system Several cell groups project to both branches of the autonomic nervous system, sometimes even the same neurotransmitter is used, eg, oxytocin neurons in the paraventricular nucleus and melanin-concentrating hormone and orexin neurons in the lateral hypothalamus project to both the DMV and SPN neurons Moreover, the appearance of third-order neurons located in the sympathetic SPN after complete sympathectomy and in the DMV after complete vagotomy illustrates the possibility that motor neurons of the sympathetic and parasympathetic system may exchange information by means of interneurons The presence of second-order neurons in prefrontal, gustatory, and piriform cortex may provide an anatomic basis for the involvement of these cortices in the cephalic insulin response The observation that second-order neurons in both vagal and sympathetic control of the pancreas contain neuropeptides that are known to play a role in food intake indicates a direct association between behavioral and autonomic functions Finally, the observation of third-order neurons in the suprachiasmatic nucleus and ventromedial hypothalamus shows the modulatory action of the time of the day and metabolic state, respectively

Autonomic responses of autistic children to people and objects

Abstract: Several recent lines of inquiry have pointed to the amygdala as a potential lesion site in autism. Because one function of the amygdala may be to produce autonomic arousal at the sight of a significant face, we compared the responses of autistic children to their mothers' face and to a plain paper cup. Unlike normals, the autistic children as a whole did not show a larger response to the person than to the cup. We also monitored sympathetic activity in autistic children as they engaged in a wide range of everyday behaviours. The children tended to use self-stimulation activities in order to calm hyper-responsive activity of the sympathetic ('fight or flight') branch of the autonomic nervous system. A small percentage of our autistic subjects had hyporesponsive sympathetic activity, with essentially no electrodermal responses except to self-injurious behaviour. We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes.

Neuroanatomical basis for first- and second-order representations of bodily states.

Abstract: Changes in bodily states, particularly those mediated by the autonomic nervous system, are crucial to ongoing emotional experience A theoretical model proposes a first-order autoregulatory representation of bodily state at the level of dorsal pons, and a second-order experience-dependent re-mapping of changes in bodily state within structures such as cingulate and medial parietal cortices We tested these anatomical predictions using positron emission tomography and a human neurological model (pure autonomic failure), in which peripheral autonomic denervation prevents the emergence of autonomic responses Compared to controls, we observed task-independent differences in activity of dorsal pons and context-induced differences in cingulate and medial parietal activity in PAF patients An absence of afferent feedback concerning autonomically generated bodily states was associated with subtle impairments of emotional responses in PAF patients Our findings provide empirical support for a theory proposing a hierarchical representation of bodily states

Role of stress in functional gastrointestinal disorders. Evidence for stress-induced alterations in gastrointestinal motility and sensitivity.

Abstract: Psychological stress is widely believed to play a major role in functional gastrointestinal (GI) disorders, especially irritable bowel syndrome (IBS), by precipitating exacerbation of symptoms. The available data clearly demonstrate that inhibition of gastric emptying and stimulation of colonic transit is the most consistent pattern in the motility response of the GI tract to acute or short-term stress. Thus, one might propose that these alterations might play a pathophysiological role in dyspeptic symptoms and alterations in stool frequency and consistency in patients with stress-related functional GI disorders. Taken together, the above-mentioned studies suggest that the colonic motor response to stress is exaggerated in IBS. There is evidence that an increased emotional response is associated with this difference in colonic, and perhaps also gastric motor responses to certain stressors. However, almost no valid data are available so far from human studies addressing the question if differences in motility responses to stress between patients with functional GI disorders and healthy subjects are due to an altered stress response associated with an imbalance of the autonomic nervous system or increased stress susceptibility. We can summarize that in experimental animals the most consistent pattern of GI motor alterations induced by various psychological and physical stressors is that of delaying gastric emptying and accelerating colonic transit. Endogenous corticotropin-releasing factor (CRF) in the brain plays a significant role in the central nervous system mediation of stress-induced inhibition of upper GI and stimulation of lower GI motor function through activation of brain CRF receptors. The inhibition of gastric emptying by CRF may be mediated by interaction with the CRF-2 receptor, while CRF-1 receptors are involved in the colonic and anxiogenic responses to stress. Endogenous serotonin, peripherally released in response to stress, seems to be involved in stress- and central CRF-induced stimulation of colonic motility by acting on 5HT-3 receptors. Taken together, the limited data available from investigations in healthy subjects and patients with functional GI disorders provide some evidence that stress affects visceral sensitivity in humans. Acute psychological stress seems to facilitate increased sensitivity to experimental visceral stimuli, if the stressor induces a significant emotional change. In summary, studies in experimental animals suggest that stress-induced visceral hypersensitivity is centrally mediated by endogenous CRF and involvement of structures of the emotional motor system, e.g. the amygdala. Stress-induced activation or sensitization of mucosal mast cells in the GI tract seem to be involved in stress-associated alterations of visceral sensitivity.

Marked Sympathetic Activation in Patients with Chronic Respiratory Failure

Abstract: The autonomic nervous system may be disturbed in chronic respiratory failure. We tested the hypothesis that there is increased sympathetic activity in patients with chronic hypoxemia. Furthermore, we examined the effect of short-term oxygen on muscle sympathetic nerve activity (MSNA) in these patients. We performed microneurography of the peroneal nerve in 11 patients with hypoxemia due to chronic obstructive pulmonary disease (COPD, n = 6) or lung fibrosis (n = 5) and in 11 healthy subjects matched for age and sex. MSNA was measured during normal breathing in all subjects. In eight patients and in seven control subjects, MSNA was also measured during nasal oxygen (4 L/min). MSNA was higher in the patients with chronic respiratory failure compared with the healthy subjects during normal breathing (61 +/- 5 versus 34 +/- 2 bursts/min, mean +/- SEM; p = 0.0002, paired t test). During oxygen administration, MSNA decreased from 63 +/- 6 to 56 +/- 6 bursts/min in the patients (p = 0.0004, ANOVA); there was no change in sympathetic activity in the control subjects. For the first time, there is direct evidence of marked sympathetic activation in patients with chronic respiratory failure. This is partly explained by arterial chemoreflex activation and may play an important role in the pathogenesis of the disease.

Hyperinsulinemia and autonomic nervous system dysfunction in obesity: effects of weight loss.

Abstract: Background—Because hyperinsulinemia acutely stimulates adrenergic activity, it has been postulated that chronic hyperinsulinemia may lead to enhanced sympathetic tone and cardiovascular risk. Methods and Results—In 21 obese (body mass index, 35±1 kg/m2) and 17 lean subjects, we measured resting cardiac output (by 2-dimensional echocardiography), plasma concentrations and timed (diurnal versus nocturnal) urinary excretion of catecholamines, and 24-hour heart rate variability (by spectral analysis of ECG). In the obese versus lean subjects, cardiac output was increased by 22% (P<0.03), and the nocturnal drop in urinary norepinephrine output was blunted (P=0.01). Spectral power in the low-frequency range was depressed throughout 24 hours (P<0.04). During the afternoon and early night, ie, the postprandial phase, high-frequency power was lower, heart rate was higher; and the ratio of low to high frequency, an index of sympathovagal balance, was increased in direct proportion to the degree of hyperinsulinemia ...

Gender differences in autonomic cardiovascular regulation: spectral, hormonal, and hemodynamic indexes.

Abstract: The autonomic nervous system drives variability in heart rate, vascular tone, cardiac ejection, and arterial pressure, but gender differences in autonomic regulation of the latter three parameters are not well documented. In addition to mean values, we used spectral analysis to calculate variability in arterial pressure, heart rate (R-R interval, RRI), stroke volume, and total peripheral resistance (TPR) and measured circulating levels of catecholamines and pancreatic polypeptide in two groups of 25 +/- 1.2-yr-old, healthy men and healthy follicular-phase women (40 total subjects, 10 men and 10 women per group). Group 1 subjects were studied supine, before and after beta- and muscarinic autonomic blockades, administered singly and together on separate days of study. Group 2 subjects were studied supine and drug free with the additional measurement of skin perfusion. In the unblocked state, we found that circulating levels of epinephrine and total spectral power of stroke volume, TPR, and skin perfusion ranged from two to six times greater in men than in women. The difference (men > women) in spectral power of TPR was maintained after beta- and muscarinic blockades, suggesting that the greater oscillations of vascular resistance in men may be alpha-adrenergically mediated. Men exhibited muscarinic buffering of mean TPR whereas women exhibited beta-adrenergic buffering of mean TPR as well as TPR and heart rate oscillations. Women had a greater distribution of RRI power in the breathing frequency range and a less negative slope of ln RRI power vs. ln frequency, both indicators that parasympathetic stimuli were the dominant influence on women's heart rate variability. The results of our study suggest a predominance of sympathetic vascular regulation in men compared with a dominant parasympathetic influence on heart rate regulation in women.

Early Spread of Scrapie from the Gastrointestinal Tract to the Central Nervous System Involves Autonomic Fibers of the Splanchnic and Vagus Nerves

Abstract: Although the ultimate target of infection is the central nervous system (CNS), there is evidence that the enteric nervous system (ENS) and the peripheral nervous system (PNS) are involved in the pathogenesis of orally communicated transmissible spongiform encephalopathies. In several peripherally challenged rodent models of scrapie, spread of infectious agent to the brain and spinal cord shows a pattern consistent with propagation along nerves supplying the viscera. We used immunocytochemistry (ICC) and paraffin-embedded tissue (PET) blotting to identify the location and temporal sequence of pathological accumulation of a host protein, PrP, in the CNS, PNS, and ENS of hamsters orally infected with the 263K scrapie strain. Enteric ganglia and components of splanchnic and vagus nerve circuitry were examined along with the brain and spinal cord. Bioassays were carried out with selected PNS constituents. Deposition of pathological PrP detected by ICC was consistent with immunostaining of a partially protease-resistant form of PrP (PrPSc) in PET blots. PrPSc could be observed from approximately one-third of the way through the incubation period in enteric ganglia and autonomic ganglia of splanchnic or vagus circuitry prior to sensory ganglia. PrPSc accumulated, in a defined temporal sequence, in sites that accurately reflected known autonomic and sensory relays. Scrapie agent infectivity was present in the PNS at low or moderate levels. The data suggest that, in this scrapie model, the infectious agent primarily uses synaptically linked autonomic ganglia and efferent fibers of the vagus and splanchnic nerves to invade initial target sites in the brain and spinal cord.

Hemispheric influence on autonomic modulation and baroreflex sensitivity.

Abstract: Several studies suggest hemispheric lateralization of autonomic cardiovascular control. There is controversy regarding which hemisphere dominates sympathetic or parasympathetic activity. Hemispheric influences on baroreflex sensitivity (BRS) have not yet been evaluated. To determine hemispheric autonomic control in epilepsy patients, we assessed cardiovascular and baroreflex modulation before and during hemispheric inactivation. For 15 patients with drug-refractory epilepsy, we analyzed autonomic heart rate (HR) and blood pressure (BP) modulation and BRS before and during left and right intracarotid amobarbital procedure (IAP). After Blackman-Tukey spectral analysis, we calculated the low-frequency (LF: 0.04-0.15 Hz) and high-frequency (HF: 0.15-0.5 Hz) power of HR and BP as well as BRS as the LF transfer function gain between BP and HR. Right hemispheric inactivation induced a significant decrease of BP and an increase of HF power of HR and BP (p < 0.05). Left inactivation increased HR, BP, and LF power of both signals and decreased BRS by nearly 30% (p < 0.05). The results confirm previous IAP studies showing sympathetic lateralization in the right hemisphere and, moreover, demonstrate parasympathetic predominance and up-regulation of BRS in the left hemisphere. In epilepsy patients, unilateral electrical activity might derange autonomic balance between both hemispheres and contribute to cardiovascular dysregulation and sudden fatalities.

Responses to laboratory psychosocial stress in postpartum women.

Abstract: Objective Lactation has been associated with attenuated hormonal responses to exercise stress in humans. This study was designed to determine the effect of lactation on hypothalamic-pituitary-adrenal axis, autonomic nervous system, and anxiety responses to psychological stress. Method The Trier Social Stress Test was administered to 24 lactating women, 13 postpartum nonlactating women, and 14 healthy control women in the early follicular phase of the menstrual cycle. Lactating women were stressed at least 40 minutes after last feeding their infant. Results ACTH, cortisol, heart rate, diastolic blood pressure, systolic blood pressure, and subjective anxiety ratings were all significantly increased in response to the psychological stress (all p Conclusions These results indicate that physiological and subjective responses to social stress are not attenuated in lactating women tested at least one hour after feeding their infant. However, enhanced vagal control of cardiac reactivity was observed in lactating women. In addition, postpartum women who did not lactate showed evidence of increased sympathetic and decreased parasympathetic nervous system tone.

Ambulatory ECG and analysis of heart rate variability in Parkinson's disease

Abstract: OBJECTIVES Cardiovascular reflex tests have shown both sympathetic and parasympathetic failure in Parkinson9s disease. These tests, however, describe the autonomic responses during a restricted time period and have great individual variability, providing a limited view of the autonomic cardiac control mechanisms. Thus, they do not reflect tonic autonomic regulation. The aim was to examine tonic autonomic cardiovascular regulation in untreated patients with Parkinson9s disease. METHODS 24 Hour ambulatory ECG was recorded in 54 untreated patients with Parkinson9s disease and 47 age matched healthy subjects. In addition to the traditional spectral (very low frequency, VLF; low frequency, LF; high frequency, HF) and non-spectral components of heart rate variability, instantaneous beat to beat variability (SD1) and long term continuous variability (SD2) derived from Poincare plots, and the slope of the power law relation were analysed. RESULTS All spectral components (p CONCLUSIONS Parkinson9s disease causes dysfunction of the diurnal autonomic cardiovascular regulation as demonstrated by the spectral measures of heart rate variability and the slope of the power law relation. This dysfunction seems to be more profound in patients with more severe Parkinson9s disease.

Central mineralocorticoid receptor blockade improves volume regulation and reduces sympathetic drive in heart failure.

Abstract: The mineralocorticoid (MC) receptor antagonist spironolactone (SL) improves morbidity and mortality in patients with congestive heart failure (CHF). We tested the hypothesis that the central nervous system actions of SL contribute to its beneficial effects. SL (100 ng/h for 28 days) or ethanol vehicle (VEH) was administered intracerebroventricularly or intraperitoneally to rats with CHF induced by coronary artery ligation (CL) and to SHAM-operated controls. The intracerebroventricular SL treatment prevented the increase in sodium appetite and the decreases in sodium and water excretion observed within a week of CL in VEH-treated CHF rats. Intraperitoneal SL also improved volume regulation in the CHF rats, but only after 3 wk of treatment. Four weeks of SL treatment, either intracerebroventricularly or intraperitoneally, ameliorated both the increase in sympathetic drive and the impaired baroreflex function observed in VEH-treated CHF rats. These findings suggest that activation of MC receptors in the central nervous system plays a critical role in the altered volume regulation and augmented sympathetic drive that characterize clinical heart failure.

Elevated Sympathetic Nervous Activity in Mice Deficient in αCGRP

Abstract: α-Calcitonin gene-related peptide (αCGRP) is a pleiotropic neuropeptide implicated in a variety of physiological processes. To better understand the biological functions of αCGRP, we developed an α CGRP -null mouse model using a gene targeting approach. Recordings of mean arterial pressure (MAP) and heart rate (HR) showed that basal MAP and HR were significantly higher in both anesthetized and conscious, unrestrained α CGRP -null mice than in corresponding wild-type mice. The elevated MAP in α CGRP -null mice was shown to be the result of elevated peripheral vascular resistance by α-adrenergic blockade with prazosin and by transthoracic echocardiogram, which revealed no significant differences between α CGRP -null and wild-type mice in the stroke volume, fractional shortening, and ejection fraction. Moreover, evaluation of autonomic nervous activity by measuring HR after pretreatment of atropine and/or atenolol and by analyzing arterial baroreceptor reflexes showed sympathetic nervous activity to be significantly elevated in α CGRP -null mice; elevated levels of urinary catecholamine metabolites and decreased HR variability in mutant mice were also consistent with that finding. These findings suggest that αCGRP contributes to the regulation of cardiovascular function through inhibitory modulation of sympathetic nervous activity.

Catheter Stimulation of Cardiac Parasympathetic Nerves in Humans A Novel Approach to the Cardiac Autonomic Nervous System

Abstract: Background Cardiac parasympathetic nerves run alongside the superior vena cava (SVC) and accumulate particularly epicardially adjacent to the orifice of the coronary sinus (CS). In animals, these nerves can be electrically stimulated inside the SVC or CS, which results in negative chronotropic/dromotropic effects and negative inotropic effects in the atria but not the ventricles. Parasympathetic nerve stimulation (PS) with 20 Hz in the CS, however, also excites the atria, thereby inducing atrial fibrillation. The present study overcomes this limitation by applying high-frequency nerve stimuli within the atrial refractory period. Using this technique, we investigated for the first time whether neurophysiological effects similar to those in animals can be obtained in humans. Methods and Results In 25 patients, parasympathetic nerves were stimulated via a multipolar electrode catheter placed in the SVC (stimulation with 20 Hz; n=14) or CS (pulsed 200-Hz stimuli; n=11). A significant sinus rate decrease and p...

Differential inhibition by botulinum neurotoxin A of cotransmitters released from autonomic vasodilator neurons.

Abstract: The role of the soluble NSF attachment protein receptor (SNARE) protein complex in release of multiple cotransmitters from autonomic vasodilator neurons was examined in isolated segments of guinea ...

Exercise training and autonomic nervous system activity in obese individuals.

Abstract: AMANO, M., T. KANDA, H. UE, and T. MORITANI. Exercise training and autonomic nervous system activity in obese individuals. Med. Sci. Sports Exerc., Vol. 33, No. 8, 2001, pp. 1287‐1291. Purpose: This study was designed to investigate the effects of 12 wk of exercise training on autonomic nervous system (ANS) in 18 obese middle-aged men (N 5 9) and women (N 5 9) (age: 41.6 6 1.2 yr; BMI: 27.3 6 0.4 kg·m 22 ; %fat: 29.6 6 1.3%, mean 6 SE). Methods: Each subject participated in an aerobic exercise training at anaerobic threshold (AT), consisting of 30 min/session, 3 times/wk, for 12 consecutive weeks. The ANS activities were assessed by means of power spectral analysis of heart rate variability (HRV) at resting condition before, at 5 wk, and after the exercise program. Results: The exercise training resulted in a significant decrease in body mass, BMI, and % fat (P , 0.01) but not in lean body mass

Long-term control of renal blood flow: what is the role of the renal nerves?

Abstract: We have developed a system for long-term continuous monitoring of cardiovascular parameters in rabbits living in their home cage to assess what role renal sympathetic nerve activity (RSNA) has in regulating renal blood flow (RBF) in daily life. Blood pressure, heart rate, locomotor activity, RSNA, and RBF were recorded continuously for 4 wk. Beginning 4-5 days after surgery a circadian rhythm, dependent on feeding time, was observed. When averaged over all days RBF to the innervated and denervated kidneys was not significantly different. However, control of RBF around these mean levels was dependent on the presence of the renal sympathetic nerves. In particular we observed episodic elevations in heart rate and other parameters associated with activity. In the denervated kidney, during these episodic elevations, the increase in renal resistance was closely related to the increase in arterial pressure. In the innervated kidney the renal resistance response was significantly more variable, indicating an interaction of the sympathetic nervous system. These results indicate that whereas overall levels of RSNA do not set the mean level of RBF the renal vasculature is sensitive to episodic increases in sympathetic nerve activity.

Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity

Abstract: Neurotransmitters can accelerate HIV-1 replication in vitro, leading us to examine whether differences in autonomic nervous system (ANS) activity might promote residual HIV-1 replication in patients treated with highly active antiretroviral therapy. Patients who showed constitutively high levels of ANS activity before highly active antiretroviral therapy experienced poorer suppression of plasma viral load and poorer CD4+ T cell recovery over 3–11 months of therapy. ANS activity was not related to demographic or behavioral characteristics that might influence pathogenesis. However, the ANS neurotransmitter norepinephrine enhanced replication of both CCR5- and CXCR4-tropic strains of HIV-1 in vitro via chemokine receptor up-regulation and enhanced viral gene expression, suggesting that neural activity may directly promote residual viral replication.

Neuropeptide expression in rat paraventricular hypothalamic neurons that project to the spinal cord

Abstract: The survival of the organism is dependent on keeping a balanced internal milieu in an ever-changing environment The process to achieve this balance is called homeostasis and it is accomplished by the consonant action of the endocrine system and the autonomic nervous system. Specific parts of the central nervous system (CNS) control these systems in response to various sensory inputs. One of the key sites for the coordinated action of these two homeostasis systems is the paraventricular hypothalamic nucleus (PVH). Tirrough its projections to the pituitary the PVH controls the release of different hormones. In addition, it projects heavily to brain stem and spinal cord autonomic centers. Furthermore, the PVH projects to the superficial layers of the spinal cord, where nerve fibers conveying pain and temperature modalities terminate. Thus, in addition to its motor control of the homeostasis system, the PVH may influence the processing of sensory inputs that are important for homeostatic regulation. The aim of this thesis was to investigate some aspects of the organization and function of the neuronal pathways projecting from the PVH to the spinal cord in the rat.Vasopressin, which is a peptide that is synthesized by PVH neurons, has been proposed to regulate several different processes in the spinal cord. However, the source of vasopressin fibers within the spinal cord has been a matter of some dispute. Thus, firstly, we investigated the distribution of neurons expressing vasopressin mRNA in the naive rat, thereby providing the first complete screening of the CNS for this neuropeptide at the mRNA level. The results confmn some earlier work, but also demonstrate several new sites of vasopressin mRNA synthesis. Some sites previously thought to produce vasopressin displayed no vasopressin mRNA. Our results show that the PVH is the only putative site of spinally-projecting vasopressin neurons in the naive rat Hence, all functions exerted by vasopressin in the spinal cord are likely to be controlled by the PVH.Secondly, we examined the neurochemical profile of the PVH neurons that project to the spinal cord. We show that 41% of these neurons express dynorphin mRNA, 20% express enkephalin mRNA, 38% express oxytocin mRNA, and 42% express vasopressin mRNA. This is the first time that dynorphin has been shown in PVH neurons with spinal projections, and the figures for the other peptides are substantially higher than what has been reported in previous shldies. In addition, we demonstrate that each of the spinal cord projecting subdivisions of the PVH displays distinct peptide expression patterns.Thirdly, we investigated the physiological effect of the PVH on nociceptive transmission in the spinal cord dorsal horn. However, with the present experimental approach we could not show a consistent effect of PVH stimulation on nociceptive neurons in the spinal dorsal horn. The varying results we achieved are ascribed to the functional heterogeneity of the PVH as revealed by our previous studies.The present data contribute to the nnderstanding of the complex organization of the PVH. The parcellation of peptide-expressing neurons into distinct spinal cord projecting subnuclei is likely to reflect distinct functional roles of these subnuclei, and may provide the anatomical basis for the ability of the PVH to control many different processes in the spinal cord The nnderstanding of the physiological profile of these different subnuclei will provide insight into the control of homeostasis.

Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects.

Abstract: A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean+/-S.E.M.) from 42+/-4 to 58+/-5 impulses/100 beats (P<0.01) and from 36+/-4 to 51+/-5 bursts/100 beats (P<0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.

The autonomic nervous system and hypertension

Abstract: It was shown that dysregulation of the cardiovascular system plays an important role in the development of arterial hypertension. Sympathetic drive can be increased mainly in cases of borderline and essential hypertension. The rise in sympathetic activity is not well balanced by the adequate increase in parasympathetic activity, even the PS tone is diminished. Relative sympathotony can occur beside the absolute sympathotony due to the decrease in the PS tone with normal or quantitatively less diminished sympathetic drive. The cause of the ANS activity dysbalance remains unknown. Probably there exist disorders of generator and modulator activities in higher levels of CNS, baroreceptor regulation and other peripheral (humoral and other) mechanisms. Adequate and appropriate recording of different cardiovascular parameters mainly during activation of ANS by maneuvers (orthostasis, Valsalva, etc.) is necessary. Beat-to-beat registrations of blood pressure (e.g. by Penaz method FINAPRES), heart rate (RR intervals) are necessary for the evaluation of short term blood pressure and heart rate fluctuations. Important information about S/PS activities and the balance in heart rate regulation can be achieved by spectral and non-linear analysis of the HR variability. Regular physical aerobic exercise increases the parasympathetic tone and is beneficial for restoration of the disordered S/PS balance in young hypertonics. It can be used as non-pharmacological treatment of arterial hypertension.