Action Of Catecholamines Research Articles

Gender Differences in the Effects of Prenatal Stress on Brain Development and Behaviour

An increased incidence of anxiety, depression and attention deficits in children has been linked to psychological stress during pregnancy. Subjection of a pregnant rat to stress at a time when the foetal limbic and hypothalamic pituitary adrenal (HPA) axes develop results in anxiogenic and depressive behaviour and learning and attention deficits in the offspring, which depend on its gender, intensity and timing of the maternal stress and behaviour being tested. Maternal stress increases corticosterone levels in the foetal brain, decreases foetal testosterone and brain aromatase activity in males, and alters brain catecholamine activity to that in females. Learning deficits, reductions in hippocampal neurogenesis, LTP and dendritic spine density in the prefrontal cortex are more readily seen in prenatally-stressed males, while anxiety, depression and increased response of the HPA axis to stress are more prevalent in females. Genders may differ in the sensitivity of developing brain areas to stress hormones.

Measuring job stress among hospital nurses: an attempt to identify biological markers.

The purpose of this study was to identify biological markers corresponding to job stress among hospital nurses. The subjects of this study were 128 nurses working at a university hospital. The NIOSH job stress questionnaire and the Miki Nurse Stressor 35-item Scale measured their job stress levels. The GHQ28 was also used to measure the subjects' general mental health status. Blood analyses for neuroendocrine function and immunity reaction were performed in order to identify biological markers of job stress. Stress is related to the plasma levels of catecholamine, cortisol, adrenocorticotrophic hormone, and natural killer cell activity, therefore these factors were measured accordingly. In consideration to circadian rhythms, blood was collected from the subjects prior to the start of the day shift. The nurses filled out the questionnaires on the day of the blood tests. In order to investigate the correlation between job stress reactions indicated by the questionnaires and the results of the blood tests, we utilized Pearson's correlation coefficient and partial correlation coefficient for which other affected items were controlled. In this study, significant correlations were found between job stress and biological factors; however, the correlations were not strong. Thus, it can be said that the biological markers associated with a specific kind of job stress remain unclear. In the future, rather than implementing a simple cross-sectional study, a longitudinal study including follow-up research will be more effective in establishing biological markers for job stress.

Catecholamine activity during drug conditioned place preference and aversion

Catecholamine activity during drug conditioned place preference and aversion

Pheochromocytoma

Pheochromocytoma (PHEO) is a chromaffin cell tumor embryologically arising from the neural crest tissue. The dominant secretory products of PHEO are catecholamines: noradrenaline (norepinephrine), adrenaline (epinephrine), and to a lesser extent dopamine. In addition to catecholamines, PHEO cells also elaborate and release several neuropeptides and inflammatory cytokines which can exert intra-adrenal and extra-adrenal systemic effects and cause characteristic clinical syndromes. In a concise review we present the intra-adrenal and extra-adrenal pathophysiologic implications of PHEO and the nuclear medicine modalities that permit functional imaging of physiological processes and help localize these tumors. The specific pathways of synthesis, metabolism, and inactivation of catecholamines (of PHEOs and paragangliomas) can be used as means to develop suitable tracers for positron emission tomography (PET) ligands. In this review we focus on imaging with PET using [(18)F]-fluorodopamine, [(18)F]-fluorohydroxyphenylalanine, [(11)C]-epinephrine, or [(11)C]-hydroxyephedrine and examine how functional imaging can often complement traditional anatomical imaging modalities and other scintigraphic techniques.

Sympathetic System Activity in Obesity and Metabolic Syndrome

Obesity is a very common disease worldwide, resulting from a disturbance in the energy balance. The metabolic syndrome is also a cluster of abnormalities with basic characteristics being insulin resistance and visceral obesity. The major concerns of obesity and metabolic syndrome are the comorbidities, such as type 2 diabetes, cardiovascular disease, stroke, and certain types of cancers. Sympathetic nervous system (SNS) activity is associated with both energy balance and metabolic syndrome. Sympathomimetic medications decrease food intake, increase resting metabolic rate (RMR), and thermogenic responses, whereas blockage of the SNS exerts opposite effects. The contribution of the SNS to the daily energy expenditure, however, is small ( approximately 5%) in normal subjects consuming a weight maintenance diet. Fasting suppresses, whereas meal ingestion induces SNS activity. Most of the data agree that obesity is characterized by SNS predominance in the basal state and reduced SNS responsiveness after various sympathetic stimuli. Weight loss reduces SNS overactivity in obesity. Metabolic syndrome is characterized by enhanced SNS activity. Most of the indices used for the assessment of its activity are better associated with visceral fat than with total fat mass. Visceral fat is prone to lipolysis: this effect is mediated by catecholamine action on the sensitive beta(3)-adrenoceptors found in the intraabdominal fat. In addition, central fat distribution is associated with disturbances in the hypothalamo-pituitary-adrenal axis, suggesting that a disturbed axis may be implicated in the development of the metabolic syndrome. Furthermore, SNS activity induces a proinflammatory state by IL-6 production, which in turn results in an acute phase response. The increased levels of inflammatory markers seen in the metabolic syndrome may be elicited, at least in part, by SNS overactivity. Intervention studies showed that the disturbances of the autonomic nervous system seen in the metabolic syndrome are reversible.

The Effects of Low Doses of Δ-9 Tetrahydrocannabinol on Reinforcement Processing in the Risky Decision-Making of Young Healthy Adults

Research suggests that risky decision-making is sensitive to neuromodulatory influences acting upon corticolimbic circuitry. However, while other evidence attests to effects of delta-9 tetrahydrocannabinol (THC) on the activity of reward pathways, relatively little is known about the possible involvement of cannabinoid activity in risky choice. In this experiment, we examined the effects of a single sublingual 5 mg dose of THC on a test of risky decision-making (requiring choices between simultaneously presented gambles differing in their magnitude of gains, magnitude of losses and the probability with which these outcomes were delivered). Tests of non-normative decision-making involving risk-aversion when deciding between gains and risk-seeking choices when deciding between losses were also included. In all, 15 healthy adults were administered 5 mg THC and placebo in a double-blind, placebo-controlled, within-subject, cross-over design. THC had three principal effects relative to placebo: (i) THC reduced choice of gambles with variable gains and losses, but increased choice of gambles with zero-expected value; (ii) THC reduced participants' attention towards losses when the probability of winning was low (and the probability of losing was high); and (iii) THC speeded participants' responses to gambles with large compared to small potential gains. These results suggest that THC mediates specific motivational processes and the processing of reinforcement cues during risky choice, perhaps reflecting altered CB1 receptor or catecholamine activity within corticolimbic pathways.

Two Cases of Transient Left Ventricular Apical Ballooning Syndrome Associated with Subarachnoid Hemorrhage

Electrocardiogram (ECG) abnormalities secondary to subarachnoid hemorrhage are well known, but the etiology remains unclear. Transient left ventricular apical ballooning syndrome is characterized by acute onset myocardial infarction-like symptoms, transient (reversible) cardiac dysfunction, and shapes resembling ampulla on left ventriculography. We managed general anesthesia for two patients with transient left ventricular apical ballooning and ECG abnormalities associated with subarachnoid hemorrhage. During anesthesia, their hemodynamic status was almost stable although their cardiac performance analyzed by transthoracic echocardiography and transesophageal cardiography was poor. Anesthetic management of this syndrome may be simplified if less cardiosuppressive anesthetic management is used. We recommend evaluating cardiac function with transthoracic echocardiography or transesophageal cardiography when an subarachnoid hemorrhage patient has ECG abnormalities.

Current Trends in Functional Imaging of Pheochromocytomas and Paragangliomas

Most pheochromocytomas/paragangliomas should be evaluated with anatomical imaging (computed tomography or magnetic resonance imaging) followed by functional imaging (nuclear medicine modalities). Functional imaging assures that the tumor is indeed a pheochromocytoma/paraganglioma and enables more thorough localization, especially detecting as many lesions as possible (in particular for metastatic disease). Functional imaging for pheochromocytomas/paragangliomas, can use radiolabeled ligands specific for pathways of synthesis, metabolism, and inactivation of catecholamines or nonspecific ligands. In an overview of the available nuclear medicine modalities, we summarize the accumulated experience and recommend when functional imaging should be applied to patients with pheochromocytoma/paraganglioma.

Effects of Methamphetamine on the Cerebellar Cortex

Methamphetamine (METH) targets monoamine nerve terminals and produces motor effects, which are related to changes in catecholamine activity within the basal ganglia. Cerebellum plays an important role in motor control, nonetheless only a few studies investigated the effects of METH in this area. In this article, we report preliminary results on protein expression in the cerebellum following METH administration. In particular, we focused on the rate-limiting catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). By using immunoblotting, we found that METH administration produces a dose-dependent increase of TH within the cerebellar cortex of mice, which is opposite to the decrease of TH within the striatum. Further investigations are needed in order to determine the time course, the cerebellar regions, the cellular (and subcellular) compartments, and the functional role related to these effects.

BALLOON INJURY ALTERS α‐ADRENOCEPTOR EXPRESSION ACROSS RAT CAROTID ARTERY WALL

alpha(1)-Adrenoceptors (AR) mediate growth factor-like activity of catecholamines on vascular smooth muscle cells (SMC) and adventitial fibroblasts. This trophic activity is strongly augmented by balloon injury, contributes significantly to subsequent proliferation, wall hypertrophy and lumen loss and is mediated by alpha(1A)- and alpha(1B)-AR. However, it is not known how injury augments adrenergic trophic activity. The aim of the present study was to examine alpha-AR expression in rat carotid artery and to test the hypothesis that balloon injury augments a(1)-AR expression. 2. Neointima, media and adventitia were isolated at various days after balloon injury of rat carotid artery and subjected to quantitative reverse transcription-polymerase chain reaction and radioligand binding. Cultured SMC were also studied. 3. Transcripts for alpha(1A)-, alpha(1B)-, alpha(1D)- and alpha(2D)-AR were expressed in different proportions in media and adventitia from uninjured carotid artery. Injury caused a reduction by as much as 85% at day 4 in all alpha-AR mRNA (but not cyclophilin) in both the media and adventitia. In both layers, expression returned to control by day 21 for alpha(2D)-AR and by day 42 for alpha(1A)-AR, but remained reduced by 25-50% for alpha(1B)- and alpha(1D)-AR at 42 days. alpha(1)-Adrenoceptor transcripts in the neointima at 21 and 42 days after injury were expressed at levels more than 80% lower than in the media or adventitia of uninjured carotid; alpha(2D)-AR mRNA was undetectable. The density of total alpha(1)-AR binding sites was similar in the media and adventitia of uninjured carotid. Density was reduced by approximately 60% in the intima-media and adventitia 21 days after injury. To examine possible mechanisms, early passaged cultured SMC were studied that express alpha(1D)- and alpha(1B)-AR at levels similar to in vivo but that do not express other alpha-AR. Basic fibroblast growth factor caused downregulation of alpha(1D)-AR mRNA and alpha(1)-AR density, without affecting mRNA half-life, whereas transforming growth factor-beta1 had no effect. Neither growth factor altered alpha(1B)-AR message expression. 4. These data demonstrate that: (i) carotid artery expresses the same four alpha-AR genes and similar total alpha(1)-AR density in the SMC media and fibroblast-rich adventitia; and (ii) injury induced enhancement of adrenergic trophic activity is not caused by upregulation of alpha(1)-AR, but, instead, is associated with a generalized reduction in alpha-AR expression.

Low Catechol-O-methyltransferase Activity in the Brain and Blood Pressure Regulation

Catecholamines (CAs) are important hormones in regulating blood pressure both in centrally and peripheral sympathetic nerve endings. Production of CAs, release and inactivation are three components to regulate CAs level. We have reported that the inactivation of CAs by catechol-O-methyltransferase (COMT) in the liver is important in high blood pressure in spontaneously hypertensive rats (SHR). In the present study, we investigated central role of COMT in hypertension. We investigated COMT activities in cerebral cortex, cerebellum, hippocampus, brain stem, hypophysis, and hypothalamus of SHR and Wistar-Kyoto (WKY) rats. COMT activities were assessed by measuring normetanephrine with the use of norepinephrine as an endogenous substrate. Membrane-bound COMT activities in cerebral cortex were significantly reduced in SHR (19.1+/-1.8 pmol/min/mg protein) compared with WKY rats (25.0+/-3.3 pmol/min/mg protein). The ratio of concentrations of normetanephrine/norepinephrine in cerebral cortex was also lower in SHR than in WKY rats. Our results suggest that there is an association between MB-COMT in cerebral cortex and blood pressure regulation.

Thermogenic action of catecholamines in human peripheral blood mononuclear cells

Isolated human peripheral blood mononuclear cells (PBMC) increase metabolic rate after bolus injections of noradrenaline or adrenaline (final concentrations ranging from 10 −5 to 10 −4 mol/l). This effect can be blocked by KCN. No autooxidation of catecholamines occurs under experimental conditions used. It is concluded that PBMC can be used as a model system for studying the mode of thermogenic action of catecholamines in human tisssues.

Dynamic strength training improves insulin sensitivity and functional balance between adrenergic alpha 2A and beta pathways in subcutaneous adipose tissue of obese subjects

The aim of this study was to investigate whether dynamic strength training modifies the control of lipolysis, with particular attention paid to the involvement of the antilipolytic adrenergic alpha 2A receptor (ADRA2A) pathway. Twelve obese men (age: 47.4+/-2.8 years; BMI: 32.7+/-0.9) were investigated during a 210-min euglycaemic-hyperinsulinaemic clamp conducted before and after 3 months of dynamic strength training. Before and during the third hour of the clamp, the lipolytic effect of a perfusion of isoproterenol or adrenaline (epinephrine) alone or associated with the ADRA2A antagonist phentolamine was evaluated using the microdialysis method of measuring extracellular glycerol concentration (EGC) in subcutaneous abdominal adipose tissue (SCAAT). In addition, biopsies of SCAAT were carried out before and after training to determine mRNA levels The training increased insulin sensitivity in adipose tissue. The decrease of EGC was more pronounced during the clamp conducted after the training period than during the clamp done in pre-training conditions. Before and after the training, catecholamines induced an increase in EGC, the increase being lower during the clamp on each occasion. The isoproterenol-induced increase in EGC was higher after the training. Adrenaline-induced lipolysis was potentiated by phentolamine after but not before the training. There were no training-induced changes in mRNA levels of key genes of the lipolytic pathway in SCAAT. In obese subjects, dynamic strength training improves whole-body and adipose tissue insulin responsiveness. It increases responsiveness to the adrenergic beta receptor stimulation of lipolysis and to the antilipolytic action of catecholamines mediated by ADRA2As.

Prospective and controlled studies of the actions of insulin and catecholamine in fat cells of obese women following weight reduction

Enlarged fat cells from obese subjects are characterised by insulin resistance and abnormal adrenergic regulation of lipolysis. The aim of the present study was to examine whether these aberrations return to normal following weight reduction. Obese women (n=25) were investigated before and 3+/-1 years (mean+/-SD) after steady-state weight reduction and compared with control women who were matched to the cases at re-examination in terms of age and BMI. Adipocyte volume, lipogenesis and lipolysis were determined in isolated subcutaneous fat cells following stimulation or inhibition at different steps of the lipolytic cascade. Weight reduction decreased fat cell volume and basal and adrenergic-regulated lipolysis rates to values that were 20-40% lower than those in control women (p=0.0002-0.03), despite the fact that percentage body fat was almost identical in the two groups of women. Fat cell volume was directly proportional to lipolysis in obese subjects, both before and after weight reduction, and in control subjects. Insulin-induced antilipolysis and lipogenesis were completely normalised after weight reduction. Body-weight-reduced obese women had low basal and catecholamine-stimulated adipocyte lipolysis, presumably due to adipose tissue hyperplasia. This could make an important contribution to body weight gain following weight loss. Adipocyte insulin resistance is secondary to obesity.

α1-Adrenoceptors as potential therapeutic targets

Adrenergic receptors belong to the seven transmembrane spanning, G-protein-coupled receptor super family, which mediate the actions of the endogenous catecholamines, adrenaline and noradrenaline (also known as epinephrine and norepinephrine). Adrenergic receptors are involved in several disease states such as hypertension, cardiac dysfunction, diabetes, glaucoma, depression, impotence and lower urinary tract disorders. This makes adrenergic receptors a valuable therapeutic target for the treatment of various disorders. Adrenergic receptors are broadly categorised into α1-,α2- and β-subtypes. Of these, α1-adrenoceptors, located in both central and peripheral nervous systems, are of great therapeutic relevance because of their important role in the contraction of smooth muscle tissue, especially in the cardiovascular system and lower urinary tract. The α1-adrenoceptor subtype has been further divided into α1A, α1B and α1D and ligands acting at these subtypes have therapeutic potential in the treatment of hypertension, stress urinary incontinence (SUI), benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). This review summarises the patent literature from 2001 to early 2005 on the development of selective ligands of the α1-adrenoceptor and its subtypes.

Instabilité hémodynamique et traitement au long cours par carbonate de lithium

Lithium is known to be responsible for many adverse events on the cardiovascular system. Among these events, it was experimentally noted that lithium could block the action of catecholamines on myocardium. The authors report the case of a patient under lithotherapy developing a myocardial infarction secondarily complicated of a severe cardiac failure. The inotropic support essential to balance hemodynamic could be raised only after lithium's stop. This example could be a clinical translation of the experimental effect previously observed.

Spontaneous diastolic contractions and phosphorylation of the cardiac ryanodine receptor at serine-2808 in congestive heart failure in rat

The role of phosphorylation of the ryanodine receptor at serine-2808 (RyRS2808) in congestive heart failure (CHF) is controversial, and effects of RyRS2808 phosphorylation on contraction are unclear. It has been reported that diastolic sarcomere length (SL) fluctuations accompany propagating contractile waves due to propagating SR Ca2+ release in trabeculae from rats with CHF. Here, we studied the influence of RyR destabilization by FK506 and isoproterenol on twitch force (Ftw) and SL fluctuations in right ventricular (RV) trabeculae. We measured phosphorylation of RyRS2808 in rats with myocardial infarction (MI) with or without beta-blockade and in rats during isoproterenol stimulation in order to assess the role of RyRS2808 phosphorylation in SL fluctuations in failing hearts. Five groups of male Lewis Brown-Norway rats were studied 3 months after MI: i) Sham; ii) MI with CHF (cMI); iii) MI without CHF; iv) metoprolol-treated MI, with and without CHF. The root mean square (RMSSL) of SL fluctuations in RV trabeculae was calculated. RMSSL increased strongly both following a short train of stimuli at 2.5 Hz and following catecholamine activation in trabeculae from MI with CHF, resulting in a decrease in Ftw in proportion to RMSSL. RyRS2808 phosphorylation was increased significantly in the left ventricle (LV; approximately 58%, P<0.05) but not in the RV (n.s.) in MI rats with CHF. FK506 tripled high frequency stimulation-induced RMSSL in nonfailing trabecula but did not further enhance RMSSL in failing trabecula. Isoproterenol increased RMSSL in nonfailing trabeculae only modestly despite a substantial increase in RyRS2808 phosphorylation in the RV (approximately 60%, P<0.05). Isoproterenol induced SL fluctuation without an increase in RV-RyRS2808 phosphorylation in failing trabeculae. Chronic beta-blockade decreased high frequency and catecholamine stimulation-induced RMSSL while RyRS2808 phosphorylation in the RV was indistinguishable from that in cMI. Acute RyRS2808 phosphorylation by itself does not cause spontaneous contractile waves owing to RyR2 destabilization. Spontaneous contractile waves in CHF are not caused by RyRS2808 phosphorylation alone, suggesting that factors other than RyRS2808 phosphorylation affect RyR function.

Alternative pathways for catecholamine action in oral motor control

Orofacial movement is a complex function performed by facial and jaw muscles. Jaw movement is enacted through the triggering of motoneurons located primarily in the trigeminal motor nucleus (Mo5). The Mo5 is located in the pontine reticular formation, which is encircled by premotor neurons. Previous studies using retrograde tracers have demonstrated that premotor neurons innervating the Mo5 are distributed in brainstem areas, and electrophysiological studies have suggested the existence of a subcortical relay in the corticofugal-Mo5 pathway. Various neurotransmitters have been implicated in oral movement. Dopamine is of special interest since its imbalance may produce changes in basal ganglia activity, which generates abnormal movements, including jaw motor dysfunction, as in oral dyskinesia and possibly in bruxism. However, the anatomical pathways connecting the dopaminergic systems with Mo5 motoneurons have not been studied systematically. After injecting retrograde tracer fluorogold into the Mo5, we observed retrograde-labeled neurons in brainstem areas and in a few forebrain nuclei, such as the central nucleus of the amygdala, and the parasubthalamic nucleus. By using dual-labeled immunohistochemistry, we found tyrosine hydroxylase (a catecholamine-processing enzyme) immunoreactive fibers in close apposition to retrograde-labeled neurons in brainstem nuclei, in the central nucleus of the amygdala and the parasubthalamic nucleus, suggesting the occurrence of synaptic contacts. Therefore, we suggested that catecholamines may regulate oralfacial movements through the premotor brainstem nuclei, which are related to masticatory control, and forebrain areas related to autonomic and stress responses.

Akute Nebenniereninsuffizienz („Addison-Krise“)

Die akute Nebennierenrindeninsuffizienz (NNR-Insuffizienz) oder adrenale Krise ist die Folge eines vital bedrohlichen Mangels an Glukound Mineralokortikoiden. Ursachlich liegt in der Mehrzahl der Falle eine primar adrenale Storung zugrunde, seltener entwickelt sich die Erkrankung sekundar bei einer hypophysaren oder hypothalamischen Lasion. Pathophysiologisch dominierend fur die Entwicklung des Kreislaufversagens ist der Mangel an Mineralokortikoiden. Gleichzeitig ist aber auch das Fehlen der mineralokortikoiden Eigenwirkung der korpereigenen Glukokortikoide von Bedeutung. Dass Glukokortikoide unabdingbar fur die Wirksamkeit von Katecholaminen sind, wurde erst in jungerer Zeit erkannt und erklart das schlechte Ansprechen der unbehandelten NNR-Insuffizienz auf die Gabe von Katecholaminen. Diagnostisch hinweisende Symptome wie Mudigkeit, Abdominalschmerzen, Ubelkeit und Fieber sowie charakteristische Laborveranderungen wie Hyponatriamie, Hyperkaliamie und Hypoglykamie ergeben sich aus der Kombination der verschiedenen Hormonmangelsituationen. Die Diagnosesicherung mittels Cortisol-, ACTH-Bestimmung und ACTH-Kurztest kann vor Therapieeinleitung in aller Regel nicht abgewartet werden. Basis der Behandlung ist die sofortige Bolusinjektion von 100 mg Hydrocortison, gefolgt von einer hochdosierten Bolus- oder Dauerinfusion (100 mg Hydrocortison alle 8–12 h) und Volumenersatz bis zur klinischen Stabilisierung. Die an dritter Stelle stehende Substitution von Mineralokortikoiden ist nur bei primarer NNR-Insuffizienz und dabei erst nach Absenken der Hydrocortisondosis auf <50 mg/d erforderlich. Selten kann es auch unter einer supraphysiologischen Glukokortikoidtherapie zum Auftreten einer adrenalen Krise kommen, insbesondere wenn die Behandlung abrupt abgesetzt oder rasch ausgeschlichen wird. In Ermangelung klinischer Studien dienen hier empirisch gewonnene Modelle und eine engmaschige klinische Verlaufskontrolle der Prophylaxe dieser vermeidbaren Nebenwirkung.

Chronic but Not Acute Hydrocortisone Treatment Shifts the Response to an Orthostatic Challenge towards Parasympathetic Activity

Adrenocortical steroid hormones play a major role in the regulation of both action and metabolism of catecholamines. However, there is limited information on the effect of prolonged increase in plasma steroid hormone concentration on the sympathetic nervous system, which is the main source of norepinephrine. Using a double-blind, placebo-controlled cross-over design, we examined 20 male healthy volunteers after acute administration of 40 mg hydrocortisone or matching placebo as well as after a 1-week treatment with this steroid (daily dose, 40 mg) or placebo. Sympathetic nervous system activity was assessed by determination of overnight urinary norepinephrine and epinephrine secretion and by analysis of short-time heart rate variability (HRV) measures in the frequency domain. The low-frequency (LF) component of the HRV spectrum was considered to reflect both sympathetic and parasympathetic modulation and the high-frequency (HF) band vagal activity. HRV testing included the response to a mild cardiovascular challenge, orthostasis. After 1 subject had been excluded because of incompliance with the study medication, the data of 19 subjects were used for further analyses. Prolonged hydrocortisone treatment was associated with a significant shift of relative power from the LF to the HF band in the upright position, resulting in a significant decrease in the LF/HF ratio (placebo 6.77 ± 3.35 and hydrocortisone 4.72 ± 3.27; p < 0.05). No differences between groups were observed after acute steroid administration or after prolonged treatment in the supine position. Neither acute nor chronic hydrocortisone treatment resulted in significant changes in the overnight urinary catecholamine secretion. Our data suggest that prolonged but not acute hydrocortisone administration shifts the autonomic response to an orthostatic challenge towards parasympathetic activity.