Number Of Β-adrenergic Receptors Research Articles

Exposure of the Gestating Mother to Sympathetic Stress Modifies the Cardiovascular Function of the Progeny in Male Rats

Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function and sensitivity to in vivo adrenergic stimulation were studied in male progeny. Pregnant Sprague-Dawley rats were exposed to cold stress (4 °C/3 h/day); rats' male progeny were euthanized at 20 and 60 days old, and their hearts were used to determine the β-adrenergic receptor (βAR) (radioligand binding) and NE concentration. The in vivo arterial pressure response to isoproterenol (ISO, 1 mg/kg weight/day/10 days) was monitored in real time (microchip in the descending aorta). Stressed male progeny presented no differences in ventricular weight, the cardiac NE was lower, and high corticosterone plasma levels were recorded at 20 and 60 days old. The relative abundance of β1 adrenergic receptors decreased by 36% and 45%, respectively (p < 0.01), determined by Western blot analysis without changes in β2 adrenergic receptors. A decrease in the ratio between β1/β2 receptors was found. Displacement of 3H-dihydroalprenolol (DHA) from a membrane fraction with propranolol (β antagonist), atenolol (β1 antagonist), or zinterol (β2 agonist) shows decreased affinity but no changes in the β-adrenergic receptor number. In vivo exposure to ISO to induce a β-adrenergic overload provoked death in 50% of stressed males by day 3 of ISO treatment. These data suggest permanent changes to the heart's adrenergic response after rat progeny were stressed in the uterus.

Neuroplasticity induction using transcranial magnetic stimulation

In this article, we have displayed the results of an analysis of modern scientific data on the induction of neuroplasticity using transcranial magnetic stimulation. We presented the multilevel neuroplastic effects of electromagnetic fields caused by transcranial magnetic stimulation (TMS). The authors of the article determined that transcranial magnetic stimulation uses variable magnetic fields to non-invasively stimulate neurons in the brain. The basis of this method is the modulation of neuroplasticity mechanisms with the subsequent reorganization of neural networks. Repeated TMS (rTMS), which is widely used in neurology, affects neurotransmitters and synaptic plasticity, glial cells and the prevention of neuronal death. The neurotrophic effects of rTMS on dendritic growth, as well as growth and neurotrophic factors, are described. An important aspect of the action of TMS is its effect on neuroprotective mechanisms. A neuroimaging study of patients with Parkinson's disease showed that rTMS increased the concentration of endogenous dopamine in the ipsilateral striatum. After rTMS exposure, the number of β-adrenergic receptors in the frontal and cingulate cortex decreases, but the number of NMDA receptors in the ventromedial thalamus, amygdala, and parietal cortex increases. These processes ultimately lead to the induction of prolonged potentiation. In response to rTMS, neuronal excitability changes due to a shift in ion balance around a population of stimulated neurons; this shift manifests itself as altered synaptic plasticity. Combinations of rTMS treatment and pharmacotherapy (e.g., small doses of memantine) may block the alleviating effect during prolonged potentiation. Studies using models of transient ischemic attack and prolonged ischemia have shown that rTMS protects neurons from death and alters the blood flow and metabolism in the brain. It has been demonstrated that TMS has a proven ability to modulate the internal activity of the brain in a frequency-dependent manner, generate contralateral responses, provide, along with the neuromodulating and neurostimulating effect, affect the brain as a global dynamic system.

Влияние премедикации с включением мексидола на уровень кортизола и количество β-адренорецепторов в послеоперационном периоде

Влияние премедикации с включением мексидола на уровень кортизола и количество β-адренорецепторов в послеоперационном периоде

Влияние премедикации с включением мексидола на уровень кортизола и количество β-адренорецепторов в послеоперационном периоде

Влияние премедикации с включением мексидола на уровень кортизола и количество β-адренорецепторов в послеоперационном периоде

Modulation of β-adrenergic receptor in rat lung after gamma irradiation

To study the effect of γ irradiation on β-adrenergic receptors of the lung. Healthy Sprague-Dawley rats were used as an animal model. Cell membrane proteins of lung tissue were harvested after the whole lung received 20 Gy of 60Co γ irradiation. 125I-labeled iodopindolol (125I-IPIN) was used as a ligand of β-adrenergic receptors. The numbers of the β-adrenergic receptors were determined by radioligand-receptor binding assay (RBA). Data were compared with irreversible blockage using antagonist bromoacetylalprenololmenthan (BAAM). The post-radiation RBA assay showed that the number of β-adrenergic receptors in lung tissue decreased at a steady rate. It decreased to 48% of the normal level at the 15th day after irradiation. At 40 days after radiation the level of β-adrenergic receptors started to increase at a steady rate and reached to the normal level around 70 days after radiation. There were significant differences in receptor synthesis, degradation and regeneration rates between irradiation group and BAMM group. The whole lung irradiation could severely affect the levels of β-adrenergic receptors. The potential clinical implications of radiation-induced changes of β-adrenergic receptors warrant further investigation.

Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo

A significant increase in cardiovascular medication use during pregnancy occurred in recent years. Only limited evidence on safety profiles is available, and little is known about the mechanisms of adverse effect on the fetus. We hypothesized that drug-induced bradycardia is the leading mechanism of developmental toxicity. Embryotoxicity was tested in ovo after administration of various doses of metoprolol, carvedilol, or ivabradine. Embryonic day (ED) 4 and 8 chick embryos were studied by video microscopy and ultrasound biomicroscopy ex ovo after intraamniotic injection of the drug for a period of 30 min. Stroke volume was calculated by the Simpson method and prolate ellipsoid formula. Significant dose-dependent mortality was achieved in embryos injected with carvedilol and ivabradine. In ED4 embryos, metoprolol, carvedilol, and ivabradine reduced the heart rate by 33%, 27%, and 55%, respectively, compared with controls (6%). In ED8 embryos this effect was more pronounced with a heart rate reduction by 71%, 54%, and 53%, respectively (controls, 36%). Cardiac output decreased in all tested groups but only proved significant in the metoprolol group in ED8 embryos. The number of β-adrenergic receptors showed a downward tendency during embryonic development. A negative chronotropic effect of metoprolol, carvedilol, and ivabradine was increasingly pronounced with embryonic maturity despite a downward trend in the number of β-adrenergic receptors. This effect was associated with reduced cardiac output in chick embryos, probably leading to premature death. Although standard doses of these drugs appear relatively safe, high doses have a potentially adverse effect on the fetus through reduced heart rate.

Not so fast: intrinsic heart rate vs. β-adrenergic responsiveness in the aging human heart

two of the fundamental observations associated with the cardiovascular responses to exercise are that heart rate increases with exercise but that maximum heart rate declines with aging. This decline in maximum heart rate with aging has a number of important consequences, including its major

Docosahexaenoic acid facilitates cell maturation and β-adrenergic transmission in astrocytes

The effects of docosahexaenoic acid (DHA; 22:6 n-3), a major omega-3 PUFA in the mammalian brain, on the structure and function of astrocytes were studied using primary cultures from rat cerebra. Gas-liquid chromatography of methyl esters of FAs isolated from cultures exposed to individual FAs, namely, stearic acid, linoleic acid, arachidonic acid, and DHA, showed alterations in the lipid profiles of the membranes, with a preferential incorporation of the FA to which the cells were exposed. Immunofluorescence studies demonstrated that unlike treatment with other FAs, after which the astrocytes remained as immature radial forms, DHA-treated astrocytes showed distinct differentiation, having morphology comparable to those grown in normal serum-containing medium. Receptor binding studies to determine the concentration of various neurotransmitter receptors showed that DHA selectively increased the number of beta-adrenergic receptors (beta-ARs) compared with FA-untreated controls, suggesting a greater role of DHA on beta-AR expression in membranes. This was also reflected by an increase in downstream events of the beta-AR pathways, such as the induction of protein kinase A and glycogen turnover by isoproterenol (ISP), a beta-AR agonist in DHA-treated cells. Moreover, ISP completely transformed DHA-treated cells into mature astrocytes bearing long processes, as in cells grown under normal conditions. Together, our observations suggest that DHA plays a unique role in facilitating some of the vital functions of astrocytes in the developing brain.

Is the upregulation of bradykinin B2 receptors by TGF-β1 one of the missing pieces in the “airway hyperresponsiveness” puzzle?

transforming growth factor (TGF)-β1 belongs to the TGF-β family of proteins corresponding to a set of pleiotropic secreted signaling molecules with unique and potent immunoregulatory properties ([10][1]). TGF-β1 is produced by every leukocyte lineage, including lymphocytes, macrophages, and

Pregnancy-induced decrease in the relaxant effect of terbutaline in the late-pregnant rat myometrium: role of G-protein activation and progesterone

The effectiveness of beta2-agonists in preterm delivery is reduced by several factors. The aim of this study was to determine the influence of late pregnancy in the uterus-relaxing effect of terbutaline in the rat in vitro. Rat uterine tissues from late pregnancy (days 15, 18, 20 and 22) were used. In vitro electrical field-stimulation (EFS) was used to evoke contractions. The radioligand-binding technique, reverse transcription-polymerase chain reaction and radioimmunoassay technique were used to determine the beta-adrenergic receptor density and mRNA level and the plasma sex hormone level, respectively. The activated G-protein level of the beta-adrenergic receptors was investigated by a radiolabelled GTP binding assay.EFS-induced contractions were inhibited by terbutaline. This effect decreased towards term with respect to both the EC50 and maximal inhibition values. A drop in plasma progesterone level was also detected. Binding studies revealed an increase in beta-adrenergic receptor number on the last day of pregnancy, which correlated with the change in receptor mRNA level. The G-protein-activating effect of terbutaline decreased continuously between days 15 and 20. Surprisingly, terbutaline decreased the G-protein activation to below the basal level on day 22. However, progesterone pretreatment set back the uterine action of terbutaline, increased the density of the beta2-adrenergic receptors and their mRNA level and increased the G-protein-activating property of terbutaline. These data provide evidence of a pregnancy-induced decrease in activated G-protein level after beta2-agonist stimulation. The decrease in plasma progesterone level has a crucial role in this process. The effects of beta2-adrenergic receptor agonists in tocolytic therapy may possibly be potentiated with progesterone.

Thermal injury and sepsis modulates β-adrenergic receptors and cAMP reponses in monocyte-committed bone marrow cells

We have previously reported that adrenergic stimulation enhances monocytopoiesis following experimental burn injury and sepsis (BI/S). In the present work we measured β-adrenergic receptor number and affinity in bone marrow committed monocyte progenitor cells (CD59 +) following BI/S. We find that BI/S treatment significantly decreased monocyte progenitor cell β-adrenergic receptors but significantly increased receptor binding affinity and isoproterenol-stimulated cAMP production. CD14 expression in macrophages derived in vitro from CD59 + cells following BI/S was significantly increased by epinephrine and this change was blocked by β 2-adrenergic receptor antagonist. PCR analysis suggests the presence of β 2- but not β 1-adrenergic receptors. Enhanced adrenergic receptor signaling in CD59 + bone marrow cells following BI/S may be important in macrophage development.

Gene Therapy in Congestive Heart Failure

Although research and development of gene therapy have encountered several difficulties in recent years, they have also begun to show potential for the treatment of acquired and inherited human diseases. Gene therapy may have wide applicability for the treatment of numerous cardiovascular diseases, including congestive heart failure (CHF), ischemic heart disease, and cardiomyopathy. CHF remains a leading cause of death and morbidity in industrialized nations, and the number of patients with CHF continues to increase as the population ages. Pharmacological therapies control symptoms, reduce left ventricular (LV) dilation, improve function, and reduce mortality. These therapies control the disease but do not cure it. Currently, however, the growing knowledge of molecular mechanisms involved in myocardial dysfunction has allowed the identification of potential therapeutic targets designed with the aim of curing CHF. Several studies in animal models have provided hope that gene therapy may be one of the future strategies for the treatment of clinical CHF. In these studies, myocardial gene transfer has been used to target at least 3 different biological pathways that play a crucial role in the pathophysiology of CHF: Intracellular calcium signaling, β1-adrenergic receptor (β1-AR) signaling, and antiapoptotic signaling. The activity of sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) is decreased in failing myocardium, and this results in abnormal Ca2+ handling.1 In an animal model of heart failure, Miyamoto et al2 showed that in vivo overexpression of SERCA2a, achieved by catheter injection of an adenovirus carrying the SERCA2a gene into the aortic root, restored systolic and diastolic function to normal levels. In another study, Muller et al3 analyzed the chronic overexpression of SERCA2a in both normal and pressure-overloaded hearts (induced by abdominal aortic banding of transgenic rats). Overexpression of SERCA2a resulted in a …

Extracts of St. John's wort and various constituents affect β-adrenergic binding in rat frontal cortex

The present study was designed to get further insight into the mode of antidepressant action of extracts prepared from St. John's wort (SJW) and relevant active constituents. Down-regulation of central β-adrenergic receptors (β-AR's) has been widely considered a common biochemical marker of antidepressant efficacy. Although previous studies have reported a β-AR down-regulation for SJW extracts, in vivo studies that compare the effects of SJW extracts with those of relevant active constituents on β-AR density have not been done yet. We used quantitative radioligand receptor-binding-studies to examine in rats the effects of short-term (2 wks) and long-term (8 wks) administration of different SJW extracts and constituents on β-AR binding in rat frontal cortex. The effects were compared to those of the standard antidepressants imipramine and fluoxetine. [ 125I]CYP binding to β-AR was found to be decreased after short as well as after long-term treatment with imipramine (36%, 40%). Short-term treatment with fluoxetine decreased the number of β-adrenergic receptors (17%) while long-term treatment with fluoxetine elicited an increase (14%) in β-AR-binding. This effect was comparable to that of the lipophilic CO 2 extract which decreased β-AR-binding (13%) after two weeks and slightly increased the number of β-AR's after 8 weeks (9%). Short-term treatment with the methanolic SJW extract decreased β-AR-binding (14%), no effects for this extract were observed after 8 weeks. Treatment with hypericin led to a significant down-regulation (13%) of β-AR's in the frontal cortex after 8-weeks, but not after 2 weeks, while hyperforin (used as trimethoxybenzoate, TMB), and hyperoside were ineffective in both treatment paradigms. Compared to the SJW extracts and single compounds the effect of imipramine on β-AR-binding was more pronounced in both treatment paradigms.

The importance of the prolonged postnatal period in determination of heart atrial muscarinic receptor and β-adrenoceptor densities

Our previous work indicated that hyperstimulation of muscarinic receptors brought about profound changes not only in the density of the muscarinic receptors, but also of the β-adrenoceptors both in vivo and in vitro. Now we try to identify the changes in receptor densities when the neuronal input from the autonomic nerves is disrupted, i.e. when neonatal rats were injected with 6-hydroxydopamine (6-OHDA; able to destroy sympathetic nerves). Although the interruption of neuronal input was successful as indicated by norepinephrine uptake, there was no change in receptor densities in the rat heart atria when 6-OHDA was applied in the first postnatal week only. When we repeated the 6-OHDA treatment consequently (on 14 th, 21 st and 28 th postnatal day) there were clear increases of both receptor types (muscarinic receptors rise to 139% of control, β-adrenoceptors to 134% of control). The atrial muscarinic receptor number was increased (to 146% of control) also when we combined the first week 6-OHDA application with another factor (when the pups abide with mother till the 56th day). The simple non-weaning of animals has no effect on the receptor densities. We can therefore conclude that the first week application of 6-OHDA was insufficient in changing the receptor number and that only repeated 6-OHDA administration was able to change them. Similarly, combination with other factor: non-weaning led to the muscarinic receptors increase. Our results can indicate the importance of the prolonged postnatal period for the heart muscarinic and β-adrenergic receptor number determination.

The effect of temperature on adrenergic receptors of alveolar type II cells of a heterothermic marsupial

Fat-tailed dunnarts, Sminthopsis crassicaudata, survive dramatic changes in body temperature during torpor without experiencing surfactant dysfunction. Adrenergic factors regulate surfactant secretion through β 2-adrenergic receptors on alveolar type II cells. Temperature has no effect on the secretory response of dunnart type II cells to adrenergic stimulation. We hypothesise that during torpor, dunnart type II cells up-regulate the number of adrenergic receptors present on type II cells to enable stimulation at lower concentrations of agonist. Here, we isolated type II cells from warm-active (35 °C) and torpid (15 °C) dunnarts and examined the effects of an in vitro temperature change on the number and activity of adrenergic receptors. Torpor did not affect the β-adrenergic receptor number. However, we observed a significant decrease in adrenergic receptor number when cells from warm-active animals were incubated at 15 °C and when cells from torpid animals were incubated at 37 °C. cAMP production was significantly higher in type II cells from torpid dunnarts than warm-active dunnarts and this may contribute, in part, to the temperature insensitivity we have previously observed in the adrenergic regulation of surfactant secretion.

Regulation of the cAMP-elevating effects of isoproterenol and forskolin in cardiac myocytes by treatments that cause increases in cAMP

Regulation of the cAMP-elevating effects of isoproterenol and forskolin in cardiac myocytes by treatments that cause increases in cAMP. We have found that elevations in cyclic AMP (cAMP) have long-term effects on both the β-adrenergic receptor and adenylyl cyclase in cultured chick ventricular myocytes. Pretreatment with isoproterenol for 15 min markedly reduced the cAMP-elevating effect of a subsequent treatment with isoproterenol 18 h later. Responses to isoproterenol were similarly reduced after overnight treatments with forskolin or phosphodiesterase inhibitors. Furthermore, these same treatments also markedly blunted the cAMP-elevating effect of forskolin, a direct activator of adenylyl cyclase. The blunting of the isoproterenol effect was greater than that of the forskolin effect, at least partially because the pretreatments caused a decrease in the number of β-adrenergic receptors as well as a net decrease in adenylyl cyclase activity. Experiments with a recombinant adenovirus to express luciferase under the control of cAMP responsive elements (CREs) showed that the same treatments elevated cAMP sufficiently to drive the transcription of a gene with CREs in its promoter. The blunting of both the isoproterenol and forskolin responses was blocked by the inhibition of protein synthesis or by infecting cells with a recombinant adenovirus that expresses rabbit muscle cAMP-dependent protein kinase inhibitor (PKI). It is hypothesized that one or more adenylyl cyclase isozymes responsible for the generation of cAMP in the myocytes, along with other proteins previously reported to regulate β-adrenergic receptors and perhaps adenylyl cyclase, are negatively regulated by cAMP, most likely at the level of gene expression, and that this regulation may have therapeutic consequences in the treatment of cardiac diseases.

Asthma and sex hormones.

A chronic in ammatory state of the airways is considered the hallmark of asthma (1). However, the incidence, severity, and prognosis of asthma can be affected by a number of factors, including the patient's sex and age. The sex of the fetus seems to in uence the development of the respiratory apparatus. In fact, between weeks 28 and 40 of gestation, the lungs are in a more advanced state in females than in males (2), a fact which could explain, at least in part, the higher incidence of respiratory distress in male infants (3). Clinical observations and epidemiologic studies agree that childhood asthma is more frequent in boys than in girls (4). Moreover, in some children, usually boys, asthmatic symptoms that started in infancy disappear around puberty (5), while many girls have the disease only during adolescence (6). Age has been implicated in the severity of asthma. Asthma beginning during adulthood is generally more severe than childhood-onset asthma (7). Asthma that starts around the menopause or in old age is generally quite severe (5). According to two recent epidemiologic investigations, the patient's sex and age affect the hospitalization rate for asthma (8, 9), which is a marker of severity. In the ®rst study (a retrospective study of 33 269 patients), the admission rate of boys in the 0±10-year age group was almost twice that of girls. In the next decade, sex differences in the hospitalization rate were irrelevant, although there was a small, but signi®cant prevalence of females. At all ages above 20 years, hospital admission rates were higher in women than men, with a female/ male ratio ranging from 3:1 in subjects aged 20±50 years to 2.5:1 in those over 50 years of age (8). Similar data were reported by Elliasson (9). Both studies found a relationship between the age and sex of the patient and the severity of the asthma attack as indicated by duration of hospitalization. In fact, the duration of hospitalization increased with age in both sexes; moreover, hospital stays were longer in women over 30 years of age than in men of the same age (8, 9). Abbreviations. FSH: follicle-stimulating hormone; LH: luteinizing hormone; NK cell: natural killer cell; IL-1, -4, -5, -6: interleukin-1, -4, -5, -6; TGF-b: tumor growth factor-beta; PEFR: peak expiratory ow rate. Allergy 2001: 56: 13±20 Printed in UK. All rights reserved Copyright # Munksgaard 2001

Modulation of Gluconeogenesis by Epinephrine in Hepatocytes Isolated from Genetically Obese (fa/fa) Zucker Rats

The obese (fa/fa) Zucker rat shows an impaired sympathetic tone which is accompanied by an altered thermogenesis and changes in both lipid and carbohydrate metabolism. In this work, we have investigated the regulatory effects of epinephrine on the rate of gluconeogenesis from a mixture of [14C]lactate/pyruvate, in hepatocytes isolated from obese (fa/fa) rats and their lean (Fa/−) littermates. Epinephrine caused a dose-dependent stimulation of the rate of [14C]glucose formation in both obese and lean rat hepatocytes, the maximal rates being five- and twofold higher than the corresponding basal values (0.50 ± 0.06 and 1.96 ± 0.15 μmol of lactate converted to glucose/g of cell × 20 min, respectively). No significant differences were found between the calculated half-maximal effective concentrations (EC50) for epinephrine in obese and lean rat liver cells. The stimulation of gluconeogenesis by epinephrine was accompanied by a decrease in the cellular concentration of fructose 2,6-bisphosphate, and an inactivation of both pyruvate kinase and 6-phosphofructo 2-kinase, to similar extents in both types of hepatocytes. Epinephrine also significantly raised the hepatocyte content of cyclic AMP, with about a twofold increase at a saturating concentration of the catecholamine (1 μM), in both lean and obese rat liver cells. However, at suboptimal concentrations of epinephrine, the rise in cyclic AMP levels was significantly less marked in obese than in lean rat hepatocytes. Nevertheless, no significant differences were found in either the affinity or the number of β-adrenergic receptors, in radioligand binding studies carried out in liver plasma membranes obtained from obese and lean Zucker rats. In conclusion, compared to the corresponding basal values, the response of gluconeogenesis from lactate to the stimulatory effect of epinephrine is higher in obese (fa/fa) than in lean (Fa/−) Zucker rat hepatocytes, with no significant differences in the calculated EC50 values for this hormone. This occurs in spite of an apparent decreased sensitivity of the adenylate cyclase system to the stimulatory effect of epinephrine in obese rat liver cells.

Effect of Secretion of Splenocytes after Superior Ovarian Nerve Section on the Ovarian Steroidogenesis

It is known that ovary and spleen are innervated extensively by afferent and efferent noradrenergic sympathetic nerve fibers from the celiac ganglion. Furthermore, immune cells located in the ovary influence the ovarian physiology. However, the peripheral interaction between the immune and neuroendocrine system is poorly understood. This work was undertaken to study the effect of superior ovarian nerve (SON) transection, in adult rats, on the number of splenocyte β-adrenergic receptors and their possible relation to ovarian steroidogenesis, measuring the effect of secretions of those splenocytes on progesterone and estradiol release from the ovary. Seven days after SON transection, the splenocytes were isolated and then cultured for 48 h. Their number of β-adrenergic receptors, measured using [¹²⁵I]-cyanopindolol as ligand, increased, and their culture media, used to stimulate ovaries from 60-day-old intact (neither SON-transected nor sham-operated) rats in vitro on diestrous day 2 showed a decrease in progesterone release and an increase in estradiol release in relation to splenocyte culture media of control rats (sham-operated; p < 0.001, respectively). The effects of in vivo SON transection were simulated by an in vitro system modulating the splenocyte β-adrenergic receptor number. The splenocytes from SON-transectioned rats were preincubated with and without norepinephrine (NE) 10^–6 M for 48 h, a low and high number of β-adrenergic receptors respectively, and then were stimulated with NE 10^–6 M for 24 h. After that, the culture medium from splenocytes with a low number of β-adrenergic receptors induced progesterone release from the ovaries of intact rats (p < 0.001), but produced no change in estradiol release. The data suggest that splenocyte secretions, which participate in the ovarian steroidogenic response, particularly in progesterone release, might be controlled by adrenergic influences since the number of splenocyte β-adrenergic receptors changes through SON-celiac ganglion-noradrenergic postganglionic innervation of the spleen. In estradiol release, probably other neurotransmitters than norepinephrine (NE) are involved when the SON is sectioned. In this paper we also show functional evidence for modulation of immune function by the sympathetic nervous system and its principal neurotransmitter, NE.

Beta-adrenergic receptor number in human lymphocytes is inversely correlated with aerobic capacity.

In the present study, the relationships between beta-adrenergic receptor (beta-AR) expression and aerobic capacity evaluated by maximal oxygen consumption (.VO2max) and oxygen consumption level at ventilatory threshold (.VO2@VT) were investigated. Seventeen physically untrained and 25 trained men participated in the study. After supine resting, the peripheral blood was sampled for preparation of lymphocytes, the model cell used to analyze the beta-AR state. The total number of beta-AR in lymphocytes (beta-ARtotal) was inversely correlated with the VO2 max (r = -0. 368; P < 0.05) and the VO2@VT (r = -0.359; P < 0.05). Similar relationships were also observed between the number of beta-AR in cell surface and both VO2 max (r = -0.491; P < 0.05) and VO2@VT (r = -0.498; P < 0.05). However, no correlation was obtained between the number of beta-AR in intracellular compartments and either VO2 max or VO2@VT. The beta2-AR mRNA level quantified by the use of competitive reverse transcription-polymerase chain reaction was inversely correlated with VO2@VT (r = -0.567; P < 0.05) and positively correlated with beta-ARtotal (r = 0.521; P < 0.05). These findings suggest that the beta-AR number in lymphocytes is inversely correlated with aerobic capacity. This relationship may be explained by downregulation of beta-AR, including internalization with subsequent degradation of the receptors and inhibition of the beta-AR biosynthesis.