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PubMed1981

[The effect of the sympathetic nervous system on cervical spondylosis (author's transl)].

A study on the effect of injury to the cervical spine, especially the so-called whiplash injury of the neck, has revealed that many patients who have sustained cervical trauma complain of, or later develop, vertigo similar to that encountered in Ménière's syndrome. Some authors offer clinical evidence to show that vertigo results from cervical nerve root irritation which is due to hypertrophic arthritis of the cervical spine and which responds to cervical traction. The etiology of this symptom-complex, however, remains unknown and, presenting a controversial problem, while some authors point out that irritation of the sympathetic nervous system may be important in this symptom (Mèniére-like syndrome, Barré-Lieou syndrome). In this study, the significance of the sympathetic nervous system in cervical spondylosis was examined. A) The effect of electric stimulation (2V, 20cps, 1msec, 1mA) of the human anterior longitudinal ligament of the cervical spine on the finger plethysmograph (PTG). This stimulation resulted in manifest alteration of PTG, such as the appearance of tense wave or contracted wave, change of pattern and tachycardia. B) Stimulation of the tissue adjacent to the cervical vertebral column which affects the sympathetic nervous system by way of the central nervous system (ventro-median nucleus of hypothalamus: VMH) was examined by using local electroencephalogram (local-EEG) of cats. By electric stimulation (4-6V, 50cps, 1msec, 1mA) of the tissue adjacent to the cervical vertebral column, local-EEG of VMH was accelerated remarkably and blood pressure was increased. Stimulation of the sciatic nerve caused moderate acceleration with excessive electric stimulation (4-10V, 20cps, 1msec, 1mA); however, stimulation of muscles of the neck and back caused no acceleration. Sensitive receptors are probably located adjacent to the cervical vertebral column. Stimulation of the sympathetic nerve may result from stimulation of the central nervous system (hypothalamus) caused by irritation resulting from excessive instability of the cervical vertebrae. The stimulation of the sympathetic nerves may be important clinically in the pathogenesis of Barré-Lieou syndrome in cervical spondylosis.

Adult↗
PubMed2002

The sympathetic nervous system: the muse of primary hypertension.

Von Euler characterised the sympathetic neurotransmitter noradrenaline (NA) and postulated that excessive neural tone was a cause of primary hypertension (PH). Thirty years ago, we found raised NA levels in 30-40% of young patients with PH. Laragh found plasma renin activity (PRA) a risk marker for coronary artery disease. With Esler, Miura, and Campese, a close association was found of plasma NA with PRA. We found raised tyrosine hydroxylase activity (AC) in the hearts of a rabbit model of sinoaortic denervated hypertension and in PH with raised plasma NA. Esler utilised titrated NA infusion and described increased spillover of NA from heart, kidney and subcortical areas of brain of patients with PH. With Eide we found raised cerebrospinal fluid (CSF) NA in PH (not secondary hypertension) and with Kolloch and Miura, we found raised plasma/CSF NA in conjunction with reduced dopaminergic tone. With Shkvatsabaya, Yurenev and Davison, we found that relaxation therapy improved the anger ambience and blood pressure of PH with raised plasma NA vs those with normal NA levels. Campese found a hypothalamic source of raised blood pressure in two rat models - microphenol treated and ischaemic kidney. The resulting hypertension was associated with raised NA turnover of their hypothalamic centres. Finally, with Hsueh and Hodis, we found raised plasma NA in association with insulin resistance increased left ventricular mass and intimal medial hypertrophy in Mexican-American diabetics and their yet unaffected offspring. Reliable estimates of human sympathetic AC, including levels of plasma NA in the effluent of selected organs and peripheral venous and arterial sites, may eventually be displaced by techniques using genetic analysis and molecular biology. Never the less, the sympathetic nervous system appears to play an important role in the pathogenesis, sequelae and therapy of PH.

Animals↗
PubMed1998

Effects of fetal and neonatal environment on sympathetic nervous system development.

The sympathoadrenal system plays an important role in the regulation of metabolic and cardiovascular activity. With respect to carbohydrate metabolism, specifically, catecholamines affect both insulin secretion and insulin action. Alterations in sympathoadrenal system function have been suggested to contribute to the constellation of disorders referred to as syndrome X (obesity, hypertension, NIDDM, and dyslipoproteinemia). The origin of any such abnormalities in sympathoadrenal function is unknown. The sympathoadrenal system, like other parts of the mammalian nervous system, is susceptible to environmental influences during development. Although these neurological alterations in rats are particularly prominent during the postpartum period, they are also apparent during intrauterine life. Moreover, the effects of these early environmental factors last well into adulthood and may represent permanent alterations in sympathetic nervous system behavior. Although the impact of maternal diabetes on sympathetic neural development has not been examined extensively, limited data available indicate that maternal diabetes may affect sympathetic nervous system development in the offspring. Although the full impact of maternal diabetes on neurological development in the offspring is unknown, given the myriad effects of the sympathoadrenal system on mammalian physiology, lasting changes in autonomic nervous system function may have potentially profound consequences for metabolic and cardiovascular regulation in adulthood.

Animals↗
PubMed1995

Relationship between sympathetic nervous system activity, baroreflex and cardiovascular effects after acute nitric oxide synthesis inhibition in humans.

OBJECTIVE: To examine the cardiovascular effects of acute systemic nitric oxide synthesis inhibition in humans in relation to the possible involvement of changes in sympathetic nervous system activity or in the baroreceptor reflex. DESIGN: Placebo or NG-monomethyl-L-arginine (250 mg by intravenous infusion for 5 min) was administered to seven healthy male volunteers according to a random, double-blind sequence. METHODS: Blood pressure and heart rate were measured non-invasively using a Finapres device from 20 min before to 80 min after starting infusion; beat-to-beat variability of blood pressure, pulse interval and systolic blood pressure and pulse interval covariation were assessed by means of spectral and sequence analysis methods. Under basal conditions and 15 min and 60 min after infusion, we measured stroke volume and indices of cardiac systolic and diastolic function by echocardiography, forearm blood flow by strain-gauge venous occlusion plethysmography, and plasma catecholamine levels. RESULTS: Compared with placebo, administration of NG-monomethyl-L-arginine caused a transient increase in blood pressure and reduction in heart rate. Stroke volume and indices of cardiac function did not change significantly, whereas cardiac index and forearm blood flow were significantly reduced after 15 min. Spectral analysis of blood pressure and pulse interval showed a significant reduction of power spectral density in the low frequencies (0.03-0.15 Hz) that persisted 60 min after infusion. The plasma noradrenaline level was significantly reduced after 15 min. No change in baroreflex engagement or sensitivity was detected by the cross-spectral or the sequence method. CONCLUSIONS: Acute systemic nitric oxide synthesis inhibition transiently increases blood pressure and reduces heart rate and cardiac index. The acute hypertensive response to NG-monomethyl-L-arginine is dependent neither on sympathetic nervous system activity, which is probably reduced as a consequence of baroreceptor reflex activation, nor on baroreceptor reflex sensitivity, which is not impaired.

Adult↗
PubMedDate not supplied

Role of the sympathetic nervous system in ethanol-induced hypertension in rats.

The present study investigated the role of the sympathetic nervous system in the development of ethanol-induced hypertension (EIH) in the rat. Sympathetic nerve activity (SNA) as an index of central sympathetic tone was measured directly from the preganglionic fibers of the greater splanchnic nerve. Four weeks after starting ethanol feeding, and prior to the development of hypertension, SNA of the ethanol-fed rats was significantly greater than that of controls. The increase in SNA was also evident at the early stages of EIH, at 8 weeks, and in fully developed EIH, after 12 weeks of ethanol consumption. Baroreceptor reflex control of heart rate (HR) but not SNA was impaired prior to the development of EIH at 4 weeks. However, at 8 and 12 weeks, baroreflex control of HR and SNA was normal or slightly greater than that of control rats. Because arterial pressure of ethanol-fed rats was significantly higher than that of controls at 8 and 12 weeks, the data suggest that ethanol feeding caused baroreceptor resetting. Pressor responsiveness to phenylephrine was depressed before the development of EIH but was similar to that of control rats following the development of EIH. The data also shows that blood and plasma volumes of ethanol-fed rats at the times that coincided with the pre- and posthypertensive states were similar to those of control rats which suggests that the development of EIH does not involve an increase in plasma volume. It is concluded that an increase in SNA contributes to the development of EIH and that baroreceptor resetting evoked by ethanol feeding plays a permissive role in maintaining an elevated blood pressure in ethanol-fed rats.

Animals↗
PubMed1997

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system.

Previous studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to 13-mmHg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. The present study was undertaken to further define the role of renal artery sympathetic nerves and the adrenal medulla in this BP increase. Male Sprague-Dawley rats had either adrenal medullectomy, bilateral renal artery denervation, or sham surgery. Rats from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left unhandled. Adrenal demedullation or renal artery denervation eliminated the chronic diurnal mean BP response (measured intra-arterially) to episodic hypoxia, whereas sham-operated controls continued to showed persistent elevation of systemic BP. Plasma and renal tissue catecholamine levels at the end of the experiment confirmed successful adrenal demedullation or renal denervation in the respective animals. The chronic episodic hypoxia-mediated increase in diurnal BP requires both intact renal artery nerves as well as an intact adrenal medulla.

Adrenal Medulla↗
PubMed1995

Contribution of the sympathetic nervous system to salt-sensitivity in lifetime captopril-treated spontaneously hypertensive rats.

OBJECTIVE: To test the hypothesis that, in lifetime captopril-treated spontaneously hypertensive rats (SHR), the sympathetic nervous system contributes importantly to the hypertensive effect of dietary sodium chloride supplementation. METHODS: Male SHR (aged 6 weeks) that had been treated from conception onward with either captopril or vehicle remained on a basal sodium chloride diet or were fed a high sodium chloride diet. After 2 weeks, the rats were subjected to ganglionic blockade and 2 days later, an infusion of clonidine. RESULTS: Lifetime captopril treatment significantly lowered mean arterial pressure in both groups. Intravenous infusion of the ganglionic blocker hexamethonium resulted in a rapid decline in MAP that eliminated the dietary sodium chloride-induced increase in MAP in both groups. Infusion of the central nervous system alpha2-adrenergic receptor agonist clonidine also resulted in a greater reduction in MAP in both groups of SHR that were fed the high (compared with the basal) sodium chloride diet. CONCLUSIONS: In both lifetime captopril-treated and control SHR, the sympathetic nervous system contributes to the pressor effects of a high sodium chloride diet.

Animals↗
PubMed1995

Influence of the sympathetic nervous system on insulin sensitivity and adipose tissue metabolism: a study in spinal cord-injured subjects.

To evaluate insulin sensitivity and adipose tissue metabolism, seven spinal cord-injured (SCI) subjects (age, 43 +/- 6 years; body mass index, 22.8 +/- 1.4; mean +/- SE) and their seven siblings (age, 45 +/- 6 years; body mass index, 24.8 +/- 0.8) were studied using oral glucose (100-g) tolerance tests (OGTTs), euglycemic insulin clamps (insulin infusion, 1 mU/kg.min), and microdialysis of the subcutaneous tissue. Blood glucose and insulin after oral glucose were significantly increased in SCI subjects as compared with their siblings. During insulin clamping, plasma adrenaline increased significantly in controls, but not in SCI subjects. However, the rates of glucose production (2.02 +/- 0.36 v 1.59 +/- 0.09 mg/kg.min) and utilization (5.13 +/- 0.71 v 5.78 +/- 0.34) were similar in the two groups. Furthermore, interstitial subcutaneous glycerol and lactate concentrations before and after oral glucose were similar in the two groups, even in neurally decentralized tissue with broken connection between the central nervous system and peripheral sympathetic nerves. The data suggest that (1) well-mobilized SCI subjects show minor insulin resistance, and (2) sympathetic nervous activity has a minor influence on adipose tissue metabolism in the postabsorptive state, but may affect insulin sensitivity during euglycemic clamping.

Adipose Tissue↗
PubMed1976

Serum dopamine beta-hydroxylase as an index of sympathetic nervous system activity in man.

Serum dopamine beta-hydroxylase (DBH) activity was comparable in eight adrenalectomized patients and in 41 normal volunteers (37.8 +/- 3.6 vs. 40.0 +/- 4.0 IU), but were very low in four patients with severe diabetic autonomic neuropathy (6.7 +/- 4.2). These observations suggest that the major source of DBH activity in human serum is probably the sympathetic nervous system. Serum DBH activity was also significantly lower in seven patients with low renin essential hypertension than in 17 patients with normal renin hypertension (19.9 +/- 4.3 vs. 43.9 +/- 5.0 IU, P less than 0.05). Dietary sodium depletion, a stimulus for catecholamine secretion, produced only a small increase in serum DBH activity in supine normal volunteers (26.5 +/- 10.4 to 33.9 +/- 11.4, P less than 0.05; n = 7) and in five adrenalectomized patients (33.0 +/- 12.7 to 44.1 +/- 15.2, P = 0.06). Plasma renin activity increased more than 3-fold in these same subjects, and did not correlate with serum DBH activity. Similarly, 4 hours of ambulation produced only a small increase in serum DBH activity which did not correlate with plasma renin activity. The small magnitude of these responses to physiological stimuli of the sympathetic nervous system diminishes the potential clinical usefulness of measurement of serum DBH activity. Further studies utilizing direct correlation of plasma and urine catecholamines with serum DBH activity are needed to establish its relationship to sympathetic nervous system activity.

Adrenal Medulla↗
PubMed2002

Involvement of the nitric oxide/L-arginine and sympathetic nervous systems on the vasodepressor action of human urotensin II in anesthetized rats.

This study examined if the nitric oxide (NO)/L-arginine pathway participates in and if the sympathetic nervous system attenuates the depressor action of human urotensin II. I.V. bolus injections of human urotensin II (0.1-30 nmol/kg) caused dose-dependent decreases in mean arterial pressure (MAP, EC(50) = 2.09 +/- 0.8 nmol/kg; Emax = -18 +/- 3 mmHg ) and increases in heart rate. The depressor response to human urotensin II (3 nmol/kg) was attenuated by approximately 50% in rats with MAP elevated through pretreatment with N(G)-nitro-L-arginine methyl ester (inhibitor of NO synthase), relative to that in rats with MAP elevated to a similar level through a continuous infusion of noradrenaline. Autonomic blockade with i.v. injections of mecamylamine (ganglion blocker) and propranolol (beta-adrenoceptor antagonist) markedly augmented the depressor response to human urotensin II, but almost completely attenuated the tachycardia. The results suggest that the depressor response to human urotensin II is partially mediated via the NO/L-arginine pathway, and is suppressed by activity of the sympathetic nervous system. Furthermore, tachycardic response to human urotensin II is primarily mediated indirectly via baroreflex mechanisms.

Adrenergic beta-Antagonists↗
PubMed2000

Change in activity of the sympathetic nervous system in diet-induced obese rats.

We investigated the change in activity of the sympathetic nervous system (SNS) in high-sucrose diet (HSD)-induced obese rats compared with controls. Power spectral analyses of R-R interval variability were performed to obtain the low frequency (LF, 0.04-0.699 Hz) and high frequency (HF, 0.7-3.0 Hz) powers. The percents of fat mass to body weight (%F/BW) and fat to muscle ratios (F/M) were significantly increased in HSD-fed rats. Plasma glucose, leptin, and triglyceride concentrations in rats fed with HSD were significantly increased. LF in normalized units (LFn), which represents both sympathetic and parasympathetic activities, was significantly increased whereas HF in normalized unit (HFn), which represents parasympathetic activity, was significantly decreased in HSD-fed rats. LF/HF, which represents sympathetic activity, was significantly increased in HSD-fed rats and was correlated with leptin (r=0.549, p<0.023), %F/BW (r=0.513, p<0.035), F/M (r=0.536, p<0.038), and triglyceride (r=0.497, p<0.042). When adjusted for leptin concentrations, however, LF/HF of HSD-fed rats was significantly decreased. In conclusion, HSD-induced obese rats showed increased LF/HF, which was significantly decreased by adjustment for leptin concentrations. We suggest that stimulating effect of leptin on SNS is reduced, which might play a role in induction of obesity by HSD.

Animals↗
PubMedDate not supplied

Vestibular influences on the sympathetic nervous system.

Studies using both electrical and natural stimulation have established that the vestibular system has prominent effects on sympathetic outflow and blood pressure. Preliminary evidence suggests that receptors in both otolith organs and semicircular canals are involved in producing these effects. Furthermore, vestibulosympathetic reflexes appear to be mediated by the medial vestibular nucleus and slowly conducting projections from the rostral ventrolateral medulla and caudal medullary raphe nuclei to preganglionic neurons in the thoracic spinal cord. However, many details are missing from our knowledge and understanding of the functional significance and neural substrate of vestibular influences on the sympathetic nervous system.

Animals↗
PubMed2000

Hypothalamic pituitary adrenocortical and sympathetic nervous system responses to the cold pressor test in Alzheimer's disease.

BACKGROUND: Increased basal activity of the hypothalamic-pituitary-adrenocortical (HPA) axis has been repeatedly demonstrated in Alzheimer's disease (AD), and some studies suggest increased basal activity of the sympathetic nervous system (SNS) in this disorder; however, the effects of AD on HPA axis or SNS responses to a standardized aversive stressor have not been examined. The neuroendocrine response to aversive stress may be relevant to the pathophysiology of AD. METHODS: Plasma adrenocorticotropic hormone (ACTH), cortisol, norepinephrine (NE), and epinephrine responses to a 1-min cold pressor test (CPT) were measured in nine medically healthy AD outpatients (age 76 +/- 2 years) and nine age- and gender-matched medically healthy cognitively normal older subjects (age 76 +/- 1 year). RESULTS: The cortisol response to CPT was increased in the AD group but the ACTH response did not differ between groups. Basal NE concentrations were higher in the AD group. Although NE responses to CPT did not differ between groups, the blood pressure response to CPT was higher in the AD subjects. CONCLUSIONS: These results suggest increased HPA axis responsiveness to CPT at the level of the adrenal cortex in AD. The results also suggest increased basal sympathoneural activity and increased cardiovascular responsiveness to sympathoneural stimulation in AD under the conditions of this experimental protocol. Increased SNS stimulatory modulation of the adrenal cortex is a possible mechanism contributing to the observed enhanced cortisol response to CPT in these AD subjects.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[Mechanism of internal inhibition (role of the sympathetic nervous system in sleep phenomena)].

It has been shown on cats that the role of the sympathetic nervous system in sleep phenomena is of an adaptive nature and is effected through chain neurohormonal reactions in which adrenaline possessing a two-phase action plays a major part: it induces excitation followed by sleep. Sleep is regarded as a variety of internal inhibition, elaborated as an adaptive reaction to the changing conditions of environment, which later becomes a behavioral reaction.

Adrenocorticotropic Hormone↗
PubMed1982

Effects of 2-deoxy-D-glucose on the cardiac sympathetic nerves and the adrenal medulla in the rat: further evidence for a dissociation of sympathetic nervous system and adrenal medullary responses.

In rats and mice, fasting suppresses and sucrose overfeeding stimulates sympathetic nervous system (SNS) activity. Fasting hypoglycemia in rats suppresses SNS activity while stimulating adrenal medullary catecholamine release. Administration of 2-deoxy-D-glucose (2-DG), an inhibitor of intracellular glucose metabolism, also stimulates the adrenal medulla. The studies reported here were undertaken to determine the SNS response to chronic 2-DG administration and to test the hypothesis that diet-induced changes in SNS activity are related to central nervous system glucose metabolism. Ingestion of 2-DG caused an increase in urinary epinephrine excretion and significant depletion of adrenal epinephrine content, both indices of adrenal medullary stimulation. Chronic sc injections of 2-DG in animals with normal or increased food consumption caused simultaneous suppression of cardiac sympathetic nerve activity, as evidenced by diminished cardiac [3H]norepinephrine turnover, and stimulation of adrenal medullary epinephrine release. Parenteral 2-DG administration to adrenalectomized rats also caused suppression of cardiac sympathetic activity. Thus, this response to neuroglycopenia is independent of adrenal medullary catecholamine release. These results indicate that central nervous system glucose metabolism may mediate diet-induced changes in SNS activity.

Adrenal Medulla↗