On the toxic effect of influenza virus on the sympathetic nervous system.
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Humans↗
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Sympathetic nervous system and blood pressure maintenance in the Brattleboro DI rat.
Experiments were performed to determine the functional role of the sympathetic nervous system (SNS) in blood pressure regulation in Brattleboro diabetes insipidus (DI) rats and to determine the effects of synthetic arginine vasopressin (AVP) on sympathetic function in DI rats. The experiments were conducted in male age-matched Long-Evans (LE) and DI rats in the conscious unstressed state. Mean arterial pressure (MAP) and heart rate were similar in conscious unstressed LE and DI rats, but basal plasma concentrations of norepinephrine (NE) and epinephrine (E) were elevated in DI rats compared with LE rats. An intra-arterial bolus injection of hexamethonium (30 mg/kg) resulted in greater reductions of MAP in DI rats (-62 +/- 5 mmHg) than in LE rats (-42 +/- 7 mmHg; P less than 0.05). Administration of AVP to DI rats by osmotic minipump reduced plasma NE concentration in DI rats to a level not different from that in LE rats, but E concentration remained elevated. AVP administration to DI rats also reduced the hexamethonium-induced fall in MAP in these animals (-47 +/- 7 mmHg) to a level not different from that in LE rats. We conclude that the SNS plays a greater role in blood pressure maintenance in conscious DI rats than in LE rats and that AVP administration can normalize plasma NE concentration and the contribution of the SNS to blood pressure maintenance in these animals.
Animals↗
Neurobiology of the stress response: contribution of the sympathetic nervous system to the neuroimmune axis in traumatic injury.
Acute injury produces an immediate activation of neuroendocrine mechanisms aimed at restoring hemodynamic and metabolic counter-regulatory responses. These counter-regulatory responses are mediated by the systemic and tissue-localized release of neuroendocrine-signaling molecules known to affect immune function. This has led to the recognition of the importance of neuroendocrine-immune modulation during acute injury as well as throughout the recovery period. The period immediately after acute injury is characterized by upregulation of proinflammatory cytokine expression leading to a later period of generalized immunosuppression. The course and progression of the host recovery from traumatic injury and the integrity of its response to a secondary challenge is directly related to the effective control of the immediate proinflammatory responses to the initial insult. Among the neuroendocrine mechanisms involved in restoring homeostasis, the sympathetic nervous system plays a central role in mediating acute counter-regulatory stress responses to injury. In addition to its recognized cardiovascular, hemodynamic, and metabolic effects, the neurotransmitters released by the sympathetic nervous system have been shown to affect immune function through specific adrenergic receptor-mediated pathways. In turn, cells of the immune system and their products have been shown to influence peripheral and central neurotransmission, leading to the conceptualization of a bidirectional neuroimmune communication system. The reflex activation of this bidirectional neuroimmune pathway in response to injury, integrated with the parasympathetic nervous system, and opioid and glucocorticoid pathways responsible for orchestrating the counterregulatory stress response, results in dynamic regulation of host defense mechanisms vital for immune competence and tissue repair. This review provides the biological framework for the integration of our understanding of the neuroendocrine mechanisms involved in mediating the stress response and their role in modulating immune function during and after traumatic injury.
Humans↗
The sympathetic nervous system in hypertension: a potential long-term regulator of arterial pressure.
UNLABELLED: INCREASED SYMPATHETIC NERVE ACTIVITY IN HYPERTENSION: Two techniques (the microneurographic method for intraneural recordings of sympathetic nerve activity and radiotracer techniques for study of norepinephrine kinetics) have been used recently to obtain sophisticated insight into regional sympathetic function in humans. Persuasive evidence now indicates that young mildly hypertensive humans have increased sympathetic neural activity. LONG-TERM REGULATION OF ARTERIAL PRESSURE: Three credible mechanisms have been proposed to sustain long-term sympathetic nervous influences in hypertension: antinatriuretic and renin stimulating effects of the renal sympathetic nerves, sympathetic influences on the development of vascular membrane properties and trophic effects of the sympathetic nerves on vascular and cardiac muscle. CONCLUSION: There is increasing evidence that the sympathetic nervous system may play a primary role in the pathogenesis of essential hypertension and the long-term regulation of arterial pressure.
Animals↗
Presence of a non-NMDA glutamate receptor subtype in the sympathetic nervous system of neonatal swine.
For the first time, the GluR-1 subtype of AMPA receptor was identified in the sympathetic nervous system of neonatal swine, an animal model of human development and heart disease. The rationale was to seek evidence of a role ascribed to glutamate in cardiorespiratory regulation in the laboratory rat. The receptor was demonstrated with the avidin-biotin immunoperoxidase technique by using an affinity-purified polyclonal antibody judged to be specific to Glu-R1 in several species. Glu-R1 immunoreactivity was regionally distributed in the thoracic spinal gray, and present intracellularly in neurons and within the surrounding neuropil. Sympathetic preganglionic neurons in the intermediolateral cell column of upper and lower thoracic spinal segments were intensely labeled and surrounded by labeled neuropil. High concentrations of Glu-R1 distinguished laminae II: substantia gelatinosa and the outer region of lamina III. Laminae I and V of the dorsal horn but not IV contained immunolabeled neurons. Arrays of moderately immunoreactive perikarya extended from an intermediate zone of laminae VII to the central gray. Glia and perivascular processes were not labeled, confirming previous observations [Tachibana, M., Wenthold, R.J., Morioka, H., Petralia, R.S., 1994. Light and electron microscopic immunocytochemical localization of AMPA-selective glutamate receptors in the rat spinal cord. J. Comp. Neurol. 344, 431-454]. Neuronal staining patterns corroborated evidence in rats indicating a postsynaptic localization of Glu-R1 associated with plasma membranes and cytoplasmic organelles [Martin, L.J., Blackstone, C.D., Levey, A.I., Huganir, R.L., Price, D.L., 1993. AMPA glutamate receptor subunits are differentially distributed in rat brain. Neuroscience 53, 327-358.; Rubio, M.E., Wenthold, R.J., 1997. Glutamate receptors are selectively targeted to postsynaptic sites in neurons. Neuron 18, 939-950]. Our data predict a role for L-glutamate in postnatal development of cardiorespiratory reflexes in swine.
Animals↗
The sympathetic nervous system is involved in the inhibitory effect of morphine on the colon motility in rats.
The role of the sympathetic nervous system in the inhibitory effect of morphine on colonic motility was investigated in male adult Wistar rats. The responses of colonic motility and blood pressure to the intravenous administration of morphine under urethane anesthesia were recorded. Sympathectomy (6-hydroxydopamine) or pretreatment with phentolamine, an alpha-adrenoreceptor antagonist (3.15 microM/kg, i.v.), or propranolol, a beta-adrenoreceptor antagonist (3.38 microM/kg, i.v.), on the inhibitory effect of intravenously administered morphine on colonic motility were observed. The results of the investigation showed that a significant depression of colonic motility occurred in untreated rats following intravenous administration of morphine, while no significant effect was seen in the sympathectomized. Pretreatment with phentolamine or propranolol also significantly attenuated the depression of colonic motility induced by morphine. Morphine also produced a transient depression of the blood pressure. However, this inhibitory effect of morphine on blood pressure was intensified after sympathectomy or pretreatment with either phentolamine or propranolol. We conclude that sympathetic activity plays an important role in the inhibitory effects of morphine on colonic motility and that both alpha- and beta-adrenoreceptors are involved.
Adrenergic Agents↗
Dysfunction of the sympathetic nervous system in cluster headache.
Ocular sympathetic function was studied in 13 cluster headache patients during and between attacks and several weeks or months after attacks had subsided. The pupillary response to tyramine eyedrops and facial sweating and flushing in response to body heating and to the taste of chilies were also investigated during remission. Pupillary dilatation lag on the symptomatic side persisted between bouts and correlated significantly with loss of thermoregulatory sweating in the lower part of the forehead. In six patients in remission, pupillary dilatation in response to tyramine eyedrops was impaired on the symptomatic side, whereas five patients showed no sign of ocular sympathetic deficit. These findings indicate that incomplete sympathetic deficit persisted on the symptomatic side in a subgroup of cluster headache patients during remission. In most of this subgroup the pattern of sympathetic deficit was consistent with impaired function of postganglionic cervical sympathetic fibres.
Adult↗
Involvement of developing sympathetic nervous system in thyroxine-mediated submandibular gland nerve growth factor and epidermal growth factor responses.
Thyroxine (T4) administration in mice during the 2nd wk of postnatal life elicits a precocious increase in submandibular gland-nerve growth factor (SMG-NGF) and epidermal growth factor (SMG-EGF) levels, but the mechanism(s) of T4 action has not been studied. The present report examines the role of the developing sympathetic nervous system (SNS) in the SMG-NGF and EGF responses to T4. For this purpose newborn mice were injected with T4 and/or 6-hydroxydopamine, a toxic congener of norephinephrine which causes selective destruction of sympathetic nerve terminals. The effectiveness of chemical sympathectomy was assessed by SMG-norepinephrine measurements using a sensitive radioenzymatic assay. The glandular norepinephrine contents were greatly reduced indicating that the dose and duration of 6-OHDA treatment were sufficient to cause a total sympathectomy in SMG tissue. In addition, the 6-OHDA treatment greatly reduced the wet weight and total protein content of the sympathetic superior cervical ganglia which innervate SMG tissue. SMG-NGF and EGF concentrations were measured by specific radioimmunoassays. 6-OHDA treatment alone did not affect the basal SMG-NGF and EGF concentrations. However, the maximal responses of SMG-NGF and EGF to T4 administration were greatly reduced by concurrent treatment with 6-OHDA. In summary, the data demonstrate a critical role for developing sympathetic nervous system in the T4-stimulated increase in SMG-NGF and EGF concentrations.
Animals↗
Hypertension caused by chronic intermittent hypoxia--influence of chemoreceptors and sympathetic nervous system.
BACKGROUND: The sleep apnea syndrome (SAS) is a common health problem with a 30% prevalence among patients with so-called essential hypertension. OBJECTIVE: Prompted by this epidemiologic link we tried to find out whether there is a cause-effect relationship between SAS and systemic hypertension. DESIGN: We developed an animal model to simulate defined aspects of the SAS. Rats were exposed to chronic repetitive hypoxia for 7 h per day and their blood pressure was measured by invasive methods. RESULTS: We found that 30 days of intermittent hypoxia sufficed for the development of a significant elevation of blood pressure. The co-exposure to hypoxia and hypercapnia had no additional effect. Surgical denervation of peripheral chemoreceptors prevented the increase in arterial blood pressure. Adrenal demedullation and chemical denervation of the peripheral sympathetic nervous system by 6-hydroxy dopamine also prevented the increase. CONCLUSIONS: Our data imply that repetitive hypoxemia in SAS is probably the cause of the high prevalence of systemic hypertension in this population and that peripheral chemoreceptors and the sympathetic nervous system play important roles in this pathophysiologic process.
Adrenal Medulla↗
The relationship between sensory and sympathetic nervous system changes and posttraumatic stress reaction following whiplash injury--a prospective study.
OBJECTIVE: To investigate differences in sensory and sympathetic nervous system (SNS) function between whiplash-injured persons with and without a posttraumatic stress reaction (PTSR). To explore associations between sensory, SNS function, and persistent PTSR at 6 months postinjury. METHODS: Seventy-six acutely (<1 month) whiplash-injured persons (10 with PTSR persisting to 6 months postinjury, 14 with early PTSR that resolved, and 52 with no PTSR) were prospectively investigated. RESULTS: Those with persistent PTSR showed sensory hypersensitivity and impaired peripheral vasoconstriction compared to those whose PTSR resolved and those without PTSR (P<.05). The early presence of sensory hypersensitivity was associated with PTSR at 6 months, but this relationship was mediated by pain and disability levels. Impaired vasoconstriction and higher pain and disability levels were associated with PTSR at 6 months. CONCLUSION: Sensory disturbances following whiplash injury are associated with persistent PTSR but may be mediated by levels of pain and disability.
Adult↗
Abnormality of the myocardial sympathetic nervous system in a patient with Becker muscular dystrophy detected with iodine-123 metaiodobenzylguanidine scintigraphy.
PURPOSE: This study was performed to determine whether I-123 metaiodobenzylguanidine (MIBG) scintigraphy can depict myocardial sympathetic nerve abnormalities in Becker muscular dystrophy. MATERIALS AND METHODS: A 34-year-old man with Becker muscular dystrophy underwent Tl-201 and I-123 MIBG scintigraphy sequentially before and 4 months after the beginning of oral administration of enalapril maleate, an angiotensin-converting enzyme inhibitor. RESULTS: Before and during treatment, stress Tl-201 scintigraphy revealed nonreversible myocardial perfusion defects in the anterior, inferoposterior, and apical walls, and I-123 MIBG scintigraphy depicted a region with decreased sympathetic nerve function or innervation. Before treatment, the I-123 MIBG heart count- mediastinum count (H:M) ratio was 2.1 and the washout rate was 21% on delayed images obtained 4 hours after the injection of I-123 MIBG, indicating hyperactivity of the sympathetic nervous system in the myocardium. During treatment, the H:M ratio was 3.0 and the washout rate was 15%. CONCLUSION: With I-123 MIBG scintigraphy it is possible to evaluate an abnormality of the myocardial sympathetic nervous system and the efficacy of administration of an angiotensin-converting enzyme inhibitor in this disease.
Adult↗
Role of sympathetic nervous system in ischemia-induced reduction of digoxin tolerance in anesthetized cats.
Acute myocardial ischemia reduces tolerance of the heart to arrhythmogenic actions of digitalis glycosides. Because both ischemia and the glycoside produce profound changes in activity of the autonomic nervous system and because sympathetic discharge or catecholamines enhance toxic actions of the cardiac glycosides, the possibility that alterations in digitalis sensitivity of ischemic heart involve changes in sympathetic nerve activity was examined using alpha-chloralose-anesthetized cats. Left anterior descending coronary artery (LAD) was completely occluded by ligation and, 40 min later, a slow i.v. infusion of digoxin was started at a rate of 1 microgram/kg/min. LAD ligation alone did not produce arrhythmias in that condition, but shortened the time to onset of digoxin-induced arrhythmias and thereby reduced the amount of digoxin required to produce the toxic manifestation. Concomitantly, digoxin concentration in plasma and nonischemic areas of the heart were lower in LAD-ligated cats at the onset of arrhythmias than those in sham-operated cats. Myocardial digoxin content in the ischemic area of the LAD-occluded heart was lower than that in nonischemic areas of the same heart. At the onset of digoxin-induced arrhythmias, Na,K-adenosine triphosphatase activity of ischemic myocardium was significantly higher than that in the nonischemic area, reflecting a lower digoxin occupancy of the glycoside binding sites on the sodium pump. Spinal cord (C1) transection or propranolol treatment prolonged the time to arrhythmias in both control and LAD-ligated cats, but failed to abolish the effect of LAD ligation to augment digoxin toxicity. Bilateral vagotomy also did not alter the enhancement of digoxin toxicity caused by ligation of LAD.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Sympathetic nervous system alterations in sleep apnea. The relative importance of respiratory disturbance, hypoxia, and sleep quality.
Numerous alterations in the sympathetic nervous system have been reported in patients with obstructive sleep apnea. It is unclear whether such alterations can be attributed to the respiratory disturbance itself, the resulting hypoxia, or disruption of sleep. We examined urinary norepinephrine levels in 45 individuals with varying amounts of respiratory disturbance and sleep disruption. All were of similar age (40 to 60 years) and body weight (100 to 160% ideal body weight), and all were free from antihypertensive medications that could influence norepinephrine levels. Twenty-four-hour urinary norepinephrine levels were correlated with respiratory disturbance index (r = 0.39, p < 0.01) and mean oxygen saturation (r = -0.36, p < 0.05). These variables, together with the time in slow-wave sleep, accounted for a statistically significant but modest percentage of the variance in urinary norepinephrine (R2 = 0.19, p < 0.05). However, the variables were so tightly intercorrelated that no single variable independently predicted norepinephrine levels in multiple regression analysis.
Adult↗
Effect of diet on sympathetic nervous system activity in chronic vitamin E-deficient rats.
This study was undertaken to examine the responsiveness of the sympathetic nervous system of chronic vitamin E-deficient rats to dietary changes. Rats receiving a vitamin E-deficient diet exhibited about 95% hemolysis after 4 weeks on the vitamin E-deficient diet and this value was maintained up to 18 months. alpha-Tocopherol in serum was not detectable in rats receiving the vitamin E-deficient diet for 18 months. Lipid peroxide concentration in serum of rats receiving the vitamin E-deficient diet for 18 months was 10-fold higher than that of control rats. Basal levels of urinary norepinephrine (NE) and epinephrine (E) excretion in chronic vitamin E-deficient rats was 2- to 3-fold higher than those of control rats. In control rats, urinary NE excretion declined during fasting and this decline was reversed upon refeeding. Urinary excretion of NE in control rats increased upon glucose feeding. However, in chronic vitamin E-deficient rats, no change was observed upon fasting and glucose feeding in either urinary NE or E excretion. These results suggest that the increase in basal levels of urinary NE excretion in chronic vitamin E-deficient rats was not influenced by dietary manipulation.
Adrenal Glands↗
The involvement of the sympathetic nervous system in meal-induced thermogenesis in mice.
The acute effect of food intake on the activity of the sympathetic nervous system (SNS) in both heart and brown adipose tissue (BAT) was investigated in mice. Upon delivery to the laboratory mice were housed singly and divided into two groups. Half the mice were accustomed to eat their daily food ration in two meals whereas the other half were given continuous access to food. SNS activity in both heart and BAT was estimated by measuring the accumulation of dopamine (DA) after having blocked the transformation of dopamine into noradrenaline (NA) with 1-cyclohexyl-2-mercapto-imidazole (CHMI). CHMI inhibits the enzyme dopamine beta-hydroxylase. On the day SNS activity was assessed, continuously fed (CF) or meal-fed (MF) mice were injected with either saline or CHMI one hour before being killed. In order to assess the anticipatory effects of being fed, a group of mice already accustomed to the meal-feeding schedule were not allowed to eat after the injections. Additional CF and MF mice were killed without being injected in order to determine the basal levels of both DA and NA. The results show that the accumulation of DA in both heart and BAT was higher in MF than CF mice regardless of whether MF mice were or were not fed after the injection of CHMI. It therefore appears that the intake of food may increase SNS activity in various tissues in mice, and that such a response may be largely of cephalic origin.
Adipose Tissue↗
Effects of MR exposure on axonal outgrowth in the sympathetic nervous system of the chick.
The effects of MR exposure on the rate and specificity of sympathetic preganglionic axonal outgrowth were examined in the chick embryo. Embryos were exposed to a static magnetic field of 1.5 T for 6 hours, 64 MHz RF field pulses, and a switched magnetic field gradient of amplitude 0.6 G/cm for 4 hours. No significant difference in axonal outgrowth was observed between MR-exposed and control embryos. In addition, the distributions of several major extracellular matrix (ECM) molecules, laminin, fibronectin, and collagen IV, were examined. Immunostaining patterns of these ECM molecules during axonal outgrowth showed no difference between MR-exposed and control embryos. Our results suggest that the MR exposure conditions used in this study do not affect axonal outgrowth in the sympathetic nervous system of the chick.
Animals↗
Hypertension in L-NAME-treated diabetic rats depends on an intact sympathetic nervous system.
We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), L-NAME (D+L), the alpha(1)- and beta-adrenergic receptor antagonists terazosin and propranolol (D+B), or L-NAME, terazosin, and propranolol (D+LB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. D+L rats had a marked, progressive increase in arterial pressure that by day 20 was approximately 60 mmHg greater than in D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in D+L rats, and chronic adrenergic receptor blockade restored the biphasic renin response in D+LB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion.
Adrenergic alpha-Antagonists↗
Epidural morphine decreases postoperative hypertension by attenuating sympathetic nervous system hyperactivity.
Twenty-four adults who were undergoing operations on the abdominal aorta were enrolled in a randomized, double-blind, placebo-controlled study in which epidural morphine sulfate (6 mg) was employed to attenuate the sympathoadrenal response to surgery to evaluate the possible contribution of sympathetic nervous system hyperactivity to postoperative hypertension. Patients who received epidural morphine required less parenteral morphine in the 24 hours following surgery, had lower analogue pain scores, and had markedly lower plasma norepinephrine levels when compared with patients in the control group who received an identical volume of saline in the epidural space. Epidural morphine had no effect on plasma epinephrine or arginine vasopressin levels. Fewer patients in the morphine group (4 of 12 vs 9 of 12 patients in the saline group) required treatment for hypertension (mean arterial blood pressure, greater than or equal to 110 mm Hg) in the 24 hours following surgery. In addition, patients in the morphine group had lower blood pressures in the 24 hours following surgery. These data suggest that sympathetic nervous system activity and not adrenal epinephrine or pituitary secretion of arginine vasopressin is responsible for the development of hypertension following aortic surgery. Furthermore, epidural narcotics appear to provide a means of attenuating this response.
Adult↗