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Effect of sympathetic nervous system on cerebral blood flow in the newborn piglet.

The role of the sympathetic nervous system on cerebral blood flow (CBF) autoregulation was evaluated in newborn piglets. Six animals were studied after ablation of the right superior sympathetic ganglion and compared to 6 control animals. Mean arterial blood pressure (MABP) was decreased by successive blood withdrawal and CBF was measured by radioactive microspheres. In denervated animals, MABP and CBF correlated positively according to a parabolic curve showing an absence of autoregulation when MABP is above 50 mm Hg (y = 0.079x2 - 5.9x + 154, p less than 0.01). In control animals, CBF remains stable throughout the experiment (y = 0.28x + 5). These data suggest a shift to the left of the upper limit of the autoregulation range in denervated animals and consequently a poor adaptation to increased MABP.

Animals↗

Thermogenesis induced by a high-carbohydrate meal in fasted lean and overweight young men: insulin, body fat, and sympathetic nervous system involvement.

OBJECTIVE: This dietary trial was designed to evaluate the effect of an experimental short-term fasting period followed by a high-carbohydrate meal on energy expenditure, thermogenesis, and sympathetic nervous system activity in normal (body mass index < 25 kg/m(2)) and overweight (body mass index > 27 kg/m(2)) men who were healthy, non-diabetic or with no other endocrine disease, non-smokers, not taking oral prescription medications, and with a stable body weight for the previous 3 mo. METHODS: Fasting and fed energy expenditures and diet-induced thermogenesis were measured after a high-carbohydrate meal in seven overweight and six lean young male subjects by indirect calorimetry. Heart rate, urinary excretion of catecholamines, serum glucose, and insulin were also measured over the experimental fasting (7.5 h) and postprandial (4 h) periods. RESULTS: After carbohydrate intake, overweight men showed a significantly higher energy production (kJ/kg of fat-free mass) than did lean individuals, and the diet-induced thermogenesis (percentage of energy intake) was positively correlated with body fat (kg), percentage of body fat, fat-free mass (kg), and fasting pre-meal serum insulin levels. Postprandial cumulative energy expenditure was directly associated with postprandial insulin response and with mean postprandial heart rate values. No significant differences in urinary catecholamines were found between lean and overweight men at basal conditions or during the study period. CONCLUSIONS: Overweight individuals showed similar short-term sympathetic nervous system responses induced by an experimental fasting period. Although diet-induced thermogenesis after carbohydrate intake was not statistically different between lean and overweight men, the postprandial insulin response and body fat content seemed to be involved in sympathetic nervous system activity.

Adipose Tissue↗

The relationship between altered blood vessel structure, hypertension, and the sympathetic nervous system.

The relationship between sympathetic innervation and arterial medial development has been examined in normotensive, hypertensive, and diabetic rats. Using the jejunal artery as a model, the number of nerve fibres innervating the artery as determined from fluorescent preparations, and the medial thickness and lumen diameter as measured from resin embedded specimens were correlated from animals prepared in various ways. The rats used were normal Sprague-Dawley (SD), SD with induced hypertension, SD with diabetes induced with streptozotocin, SD sympathectomized with 6-hydroxydopamine, spontaneously hypertensive rats (SHR), SHR treated with capsaicin to prevent hypertension development, Wistar Kyoto rats (WKY), and WKY treated with capsaicin. Examination of the jejunal arteries from these rats at 12 weeks of age following normal development, or 8 weeks of hypertension development, or 8 and 12 weeks of diabetes, showed that increased innervation occurred in the SHR under all conditions, and in the diabetic rats after 8 weeks of diabetes. Medial hypertrophy occurred in the SHR and in the SD hypertensive only. It is concluded that the special relationship which exists between the sympathetic innervation and arterial media in the SHR does not occur during hypertension development in the SD rat, nor is it necessary for normal medial development in the SD rat. The sympathetic innervation does appear to have a trophic influence on vascular smooth muscle of diabetic rats, at least in the early stages of the disease.

Animals↗

The sympathetic-nervous-system defect in primary orthostatic hypotension.

We sought to elucidate further the neurologic defect of idiopathic orthostatic hypotension, which appears to represent two distinct clinical entities. While recumbent, patients with multiple central-nervous-system defects, as well as peripheral autonomic nervous dysfunction, have normal plasma levels of norepinephrine that fail to increase normally after standing or exertion (P less than 0.001 by t-test as compared to controls). While recumbent, patients with peripheral autonomic insufficiency without signs of central-nervous-system defects have low levels of plasma norepinephrine (P less than 0.001) that also fail to increase normally after standing or exercising (P less than 0.001). Both groups have low levels of plasma dopamine-beta-hydroxylase (P less than 0.02). These findings are consistent with other pathological and pharmacologic observations suggesting that patients with central-nervous-system disease are unable to activate appropriately an otherwise intact sympathetic nervous system, whereas in patients without signs of central-nervous-system disease the deficit affects peripheral sympathetic nerves.

Adult↗

[Tumors of the peripheral sympathetic nervous system in childhood. Immunohistochemical study].

Twenty tumors of the peripheral sympathetic nervous system were investigated using a spectrum of antibodies against vimentin, neurofilament triplet, S-100 protein, neuronal specific enolase (NSE), chromogranin, synaptophysin, and vasoactive intestinal polypeptide. There were two ganglioneuromas, seven stroma rich neuroblastomas (composite ganglioneuroblastomas), five undifferentiated and six differentiating stroma poor neuroblastomas (NB) included in the series. Formalin-fixed, paraffin embedded material was used. The results showed that reactivity of the antibodies was relatively high, except the reactivity against synaptophysin. The tumor cell population showed a heterogeneous positivity in all cases. Only some undifferentiated NB were positive with the employed antibodies, which reduces the diagnostic benefit in a group of NB in which diagnostic demands of the immunohistochemistry are most important. The best results in undifferentiated NB were obtained with polyclonal antibody against NSE. This antibody is, however, not specific. Positive results of the immunohistochemistry in this group of tumors should be evaluated with caution.

Child↗

Stress, the sympathetic nervous system and hypertension.

Stress may be an important contributor to the pathogenesis of idiopathic (essential) hypertension. The probable pathway involves activation of the sympathetic nervous system and thereby an increase in peripheral resistance. This paper reviews the hemodynamics of early hypertension and attempts to relate them to stress-mediated overactivity of the sympathetic nervous system. Attention is also given the relations between obesity, race, sex and geography to hypertension.

Adult↗

The suprachiasmatic nucleus controls the circadian rhythm of heart rate via the sympathetic nervous system.

The mammalian suprachiasmatic nucleus (SCN) controls a wide variety of circadian behavioral and physiological processes. The specific motor output pathway(s) by which these diverse processes are controlled are unknown. The only established motor output of this system is the regulation of pineal melatonin synthesis via the sympathetic nervous system. It is therefore possible that other peripheral circadian rhythms are regulated similarly. To address this issue, body temperature (BT), general activity (GA), wheel-running activity (WR), and heart rate (HR) were recorded in laboratory rats, and the effects of SCN lesion (SCNX) and of pharmacological sympathectomy with guanethidine (GUAN) on these multiple circadian rhythms were determined. The SCNX abolished circadian patterns in all motor outputs, whereas sham animals showed robust rhythms in all measures. In contrast, guanethidine, which depleted peripheral but not central catecholamine content, selectively reduced HR circadian rhythmicity. Other rhythms (BT, GA, and WR) were unaffected. These results suggest that the SCN influences some peripheral targets via circadian regulation of the sympathetic nervous system, and other circadian outputs are regulated via different, unknown pathways.

Animals↗

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system.

Splenic nerve denervation abrogates enhanced splenic cytokine gene expression responses to acute heating, demonstrating that hyperthermia-induced activation of splenic sympathetic nerve discharge (SND) increases splenic cytokine gene expression. Hypothermia alters SND responses; however, the role of the sympathetic nervous system in mediating splenic cytokine gene expression responses to hypothermia is not known. The purpose of the present study was to determine the effect of hypothermia on the relationship between the sympathetic nervous system and splenic cytokine gene expression in anesthetized F344 rats. Gene expression analysis was performed using a microarray containing 112 genes, representing inflammatory cytokines, chemokines, cytokine/chemokine receptors and housekeeping genes. A subset of differentially expressed genes was verified by real-time RT-PCR analysis. Splenic SND was decreased significantly during cooling (core temperature decreased from 38 to 30 degrees C) in splenic-intact rats but remained unchanged in sham-cooled splenic-intact rats (core temperature maintained at 38 degrees C). Hypothermia upregulated the transcripts of several genes, including, chemokine ligands CCL2, CXCL2, CXCL10, and CCL20, and interleukins IL-1alpha, IL-1beta, and IL-6. Gene expression responses to hypothermia were similar for the majority of cytokine genes in splenic-intact and splenic-denervated rats. These results suggest that hypothermia-enhanced splenic cytokine gene expression is independent of splenic SND.

Animals↗

Interrelation between plasma kinin and the sympathetic nervous system in normal subjects.

To investigate the relationship between plasma kinin and the sympathetic nervous system, we measured plasma kinin, norepinephrine, and angiotensin-I-converting enzyme (ACE:kininase II) activity in normal subjects. In six normal subjects, subpressor and pressor doses of norepinephrine (10 ng/kg/min and 50 ng/kg/min, respectively) were infused for 1 hour. In five normal subjects, 60-degree head-up tilting was performed for 20 minutes. After norepinephrine infusion, plasma kinin levels were decreased significantly (p less than 0.01) with the subpressor dose of norepinephrine and were further decreased (p less than 0.01) with the pressor dose. Plasma ACE activity, however, showed no significant changes following these infusions. During the tilting, plasma kinin levels decreased significantly (p less than 0.01), whereas plasma norepinephrine levels increased significantly (p less than 0.01). From these results, the assumption of elevated levels in plasma endogenous or exogenous norepinephrine leads to a decrease in plasma kinin levels; this suggests that these two systems may be closely interrelated.

Adult↗

[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension].

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

[Thermometry as a method of evaluating the status of the peripheral sympathetic nervous system in patients with hemorrhagic fever with nephrotic syndrome].

The inference on irritation of sympathetic nervous system and predominant location of the the process in the thoracic and iliac parts of the sympathetic chain is drawn from investigation of skin temperature at various sites of the body and catecholamines excretion in 30 patients with hemorrhagic fever and renal syndrome. Norepinephrine, excretion enhancement and changes in the picture of skin temperatures were the underlying evidence.

Hemorrhagic Fever with Renal Syndrome↗

The role of the peripheral sympathetic nervous system in the natriuresis following central administration of an I1 imidazoline agonist, moxonidine.

1. Central administration of the I1-imidazoline receptor agonist moxonidine increases sodium excretion without alteration of blood pressure. In the present study we determined whether this natriuretic action was mediated through a decrease in activity of the sympathetic nervous system, as has been reported for the antihypertensive action of this compound. Interruption of the sympathetic nervous system was achieved with prazosin (alpha 1-adrenoceptor antagonist) and renal denervation. 2. In pentobarbitone-anaesthetized Sprague-Dawley rats, intracerebroventricular (i.c.v.) injection of moxonidine alone increased urine volume and sodium excretion. Prazosin (0.15 mg kg-1, i.v.) alone decreased urine flow rate and sodium excretion as compared to the vehicle controls. In the presence of prazosin, i.c.v. injection of moxonidine failed to increase sodium excretion or urine volume as compared to animals which received the prazosin alone. 3. The administration of moxonide (i.c.v.) to sham renal-denervated animals caused an increase in urine flow rate, urine sodium excretion, osmolar clearance and free water clearance. The increase in sodium excretion and osmolar clearance were completely attenuated in renal denervated rats, however, urine flow rate was still increased and this was secondary to the increase in free water clearance which remained intact. 4. These results indicate the importance of an intact sympathetic nervous system in the renal response to i.c.v. moxonidine. Moreover, the differential antagonism of these interventions on solute and water excretion indicate that they may be mediated at two separate sites and/or receptors following i.c.v. moxonidine.

Adrenergic alpha-1 Receptor Antagonists↗

Effect of hypercalcemia on renal sympathetic nervous system activity.

Since calcium plays a modulatory role in the activity of the sympathetic nervous system (SNS), in these studies, we have tested the hypothesis that hypercalcemia may alter renal SNS activity, and, consequently, renal function. Acute hypercalcemia was induced in Sprague-Dawley rats by infusion of calcium 30 mg/kg/2 h in 0.45% saline. A control group of rats received only 0.45% saline. Two more groups of rats received either calcium or 0.45% saline 7-10 days after total renal denervation. Calcium infusion increased serum calcium by 1.8 +/- 0.23 mg/dl in rats with intact renal nerves and by 2.7 +/- 0.48 mg/dl in renal denervated rats. Mean arterial pressure and inulin clearance did not change during calcium or 0.45% saline in rats with intact renal nerves. Renal sympathetic nerve activity (RSNA) decreased by 44% in rats infused with calcium, but it did not change in control animals. Calcium caused a significantly greater rise in urine volume, sodium excretion and fractional excretion of sodium than the infusion of 0.45% saline. Rats with renal denervation manifested greater baseline urine volume, sodium excretion and fractional excretion of sodium than rats with intact renal nerves. Infusion of calcium, however, caused no further rise in urine sodium excretion in these animals. alpha-Methyltyrosine, an inhibitor of norepinephrine (NE) synthesis, also increased natriuresis in rats. Calcium reduced by 27% the NE content in the kidney but not in the heart. Methyltyrosine, on the other hand, reduced NE content in both the heart and the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Sleep apnoea and sympathetic nervous system activity: a review.

A review was made of the literature relating sleep apnoea to sympathetic nervous system (SNS) activity, as inferred from catecholamine levels or muscle sympathetic nerve activity (MSNA). Twenty-four studies were located. Most studies reported an elevation of norepinephrine and MSNA, both during sleep and wakefulness among individuals with sleep apnoea. However, studies rarely controlled for known confounders of sympathetic activity, making the validity of the findings questionable.

Arousal↗

Clinical features of algodystrophy: is the sympathetic nervous system involved?

There is a spectrum of conditions which have in common burning pain, often with hyperpathia, hyperalgesia, vasomotor and sudomotor changes. When due to major nerve damage, the condition is known as causalgia; when due to minor nerve damage or other factors, various terms such as algodystrophy or reflex sympathetic dystrophy are employed. Radiography and isotopic bone scanning may be helpful investigations, and procedures which interrupt the local sympathetic nervous system are those most likely to help the pain. The classical view that the peripheral sympathetic nervous system is involved in generation of pain is questioned, and the possible roles of the central nervous system and of non-adrenergic mechanisms are summarised. That pain could be due to dysfunction of the polymodal nociceptor neurone is considered.

Humans↗