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PubMed1987

Sympathetic nervous system mediates urinary kallikrein excretion in conscious rats.

1. The influence of the sympathetic nervous system on urinary kallikrein excretion (UKal) was investigated in conscious rats during stress produced by inserting a silastic catheter through the urethra into the bladder. The effect of this stress on blood glucose (BG), mean arterial pressure (MAP), urinary volume (Uv), urinary sodium (UVNa), and glomerular filtration rate (GFR) was also studied. 2. In intact animals stress of 120 min duration produced a non-significant increase of MAP, a significant increase of BG and a decrease of UNa (P less than 0.001 t-test, 9 d.f.), but it did not affect Uv and GFR. In stressed rats UKal was considerably lower (52 milli Amidasic Units [mAU] per 100 g bodyweight, s.e.m. = 5, n = 6) than in control rats (170 mAU per 100 g, s.e.m. = 21, n = 5). The inhibitory effect on UKal was also observed when kallikrein was measured by the kininogenase method. 3. Adrenal medullectomy, performed 1 week before the experiment, suppressed the stress hyperglycaemia but did not affect the reduction of urinary kallikrein or the anti-natriuresis. 4. Intracerebroventricular (i.c.v.) injection of saline also had no effect in the control or in the stressed rats, while i.c.v. d-l-propranolol decreased MAP, suppressed the stress hyperglycaemia and the anti-natriuresis and stimulated UKal, without changes in Uv and GFR. Non-stressed control rats i.c.v. injected with saline excreted considerably less kallikrein than rats i.c.v. injected with d-l-propranolol (control saline: 162, s.e.m. = 14, n = 6; vs control d-l-propranolol: 559, s.e.m. = 20, n = 6). Even in stressed rats this difference was registered (stressed saline: 56, s.e.m. = 8, n = 6; vs stressed d-l-propranolol: 554 mAU per 100 g, s.e.m. = 33, n = 6). 5. Peripheral sympathectomy with 6-hydroxydopamine (6-OHDA) did not suppress the hyperglycaemic response to stress, but it stimulated UKal. Kallikrein excretion was similar in 6-OHDA stressed (534 mAU per 100 g, s.e.m. = 30, n = 6) than in 6-OHDA control rats (491 mAU per 100 g, s.e.m. = 34, n = 6). No differences were observed on UNa and GFR between control 6-OHDA treated rats and stressed 6-OHDA treated rats. 6. The present results suggest strongly that urinary kallikrein excretion is modulated by sympathetic activity. Results after central beta-adrenergic blockade and peripheral sympathectomy led to the hypothesis that normal sympathetic tone in the kidney inhibits the release of kallikrein into the urine.

Adrenal Medulla↗
PubMed1991

[Roles of the sympathetic nervous system in the local release of vasoactive intestinal polypeptide (VIP) from the small intestine of anesthetized dogs].

To investigate roles of the sympathetic nervous system in the local release of VIP, pharmacological alpha (phenoxybenzamine), beta (propranolol) adrenergic blockade or surgical sympathectomy by the ganglionectomy of splanchnic plexus was performed in anesthetized dogs. Portal and venous plasma VIP levels during intrajejunal infusion of 0.1 N HCl solution at a rate 1.5 ml/min for 20 minutes were observed before and after these procedures. The plasma VIP levels during the intrajejunal HCl infusion were significantly increased after blocking of alpha-adrenoceptors and surgical sympathectomy but showed no change after blocking of beta-adrenoceptors. These results suggest the inhibitory mechanism of the sympathetic nervous system on the local release of VIP from the canine small intestine. In addition, the increase of portal blood flow and bile secretion, and the elevation of bicarbonate concentration in the secreted bile during the intrajejunal HCl infusion were significantly higher after surgical sympathectomy than before, and plasma VIP levels were also significantly higher.

Anesthesia↗
PubMed1981

[Determination of plasma catecholamine as a quantitative index for the evaluation of sympathetic nervous system function in man during methacholine test (author's transl)].

For many years blood pressure has been only an index among a number of physiological conditions presenting sympathetic nervous systems activities in methacholine test due largely to the lack of specific and practical method for the determination of catecholamine. We found that methacholine induced a significant increase in plasma catecholamines with an alternation in hemodynamic change in the present study by the use of high speed liquid chromatography and automated THI method. The increments in plasma catecholamines were not correlated with apparent decrements in blood pressure. Therefore the increments in plasma catecholamines induced by methacholine were not attributable to reflex responses to hemodynamic changes and rather could be the direct effect of methacholine on sympathetic neuron and adrenal medullae. Besides there was no correlation between the increments in plasma catecholamines and methacholine indices. These data question the suitability of blood pressure as an index for the evaluation of sympathetic nervous system function during methacholine test and suggest that plasma catecholamines might be a proper parameter for the sympathetic nervous activities response to methacholine.

Adult↗
PubMed1982

Reduced sympathetic nervous system activity in rats with ventromedial hypothalamic lesions.

To determine if alterations in sympathetic nervous system (SNS) activity occur in rats with ventromedial hypothalamic (VMH) lesions, norepinephrine (NE) turnover rates were examined in various tissues of lesioned and control, weanling rats. VMH-lesioned rats fed a high-carbohydrate diet ad libitum for 4 weeks following surgery were not hyperphagic, but they gained 50% more body energy than control rats. VMH lesions extended the half-life of 3H-NE in interscapular brown adipose tissue (BAT) by 42%, in abdominal white adipose tissue (WAT) by 201%, in heart by 61% and in pancreas by 85%, and reduced total NE turnover (ng/organ/hr) in BAT (38%), WAT (57%), heart (30%) and pancreas (53%). Reduced SNS activity in BAT is consistent with the decreased energy expenditure (heat production) and increased energy efficiency observed in VMH-lesioned rats. In WAT, decreased SNS activity coupled with hyperinsulinemia would facilitate energy storage as fat by reducing lipid mobilization. In the pancreas, reduced SNS activity would contribute to hyperinsulinemia. These results support the hypothesis that VMH lesions decrease SNS activity in several organs. This change in autonomic tone is very likely a major factor in the development of obesity in VMH-lesioned animals.

Adipose Tissue↗
PubMed1979

Effect of inhibition of prostaglandin synthesis on sympathetic nervous system function in man.

The effect of inhibition of prostaglandin synthesis by indomethacin on the function of the peripheral sympathetic nervous system was studied in eight normotensive subjects. Sympathetic nervous function was assessed by measurement of plasma norepinephrine, alpha-adrenergic receptor sites on platelet membranes, and urinary excretion of epinephrine and norepinephrine. Treatment with indomethacin for 7 days resulted in significant decreases in basal plasma norepinephrine from 134 +/- 7 to 99 +/- 6 (SEM) pg/ml (P less than 0.01), a 26% decrease. Posturally stimulated norepinephrine concentrations (337 +/- 14 pg/ml in control studies) were 255 +/- 18 pg/ml (P less than 0.02), 25% lower, with indomethacin. Plasma norepinephrine after 5-min compression of hand grip (468 +/- 47 pg/ml in control) was 331 +/- 30 pg/ml (P less than 0.005), 29% lower, with indomethacin. The number of platelet alpha-adrenergic receptor sites did not change with indomethacin, nor did prostaglandin E1-stimulated cAMP production by platelet membranes. In addition, indomethacin produced no change in urinary excretion of norepinephrine or epinephrine. It is suggested that inhibition of prostaglandin synthesis may lead, via baroreceptor feedback, to a decrease in plasma norepinephrine concentration.

Adult↗
PubMed2001

Sympathetic nervous system overactivity in hypertensive patients with chronic renal failure--role of upright body position.

OBJECTIVE: The renal functional consequences of an activated sympathetic nervous system and plasma atrial natriuretic hormone (ANP) in various renal diseases are not well described. We hypothesize that norepinephrine (NE) and ANP have antagonizing effects on renal hemodynamics in diseased kidneys. MATERIAL AND METHODS: Plasma NE, ANP. glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and mean arterial pressure (MAP) were measured in the upright position in healthy controls (n = 9) and hypertensive patients with reduced GFR (n =11). The same parameters were compared between healthy controls (n = 6) and hypertensive patients with reduced GFR (n = 6) in upright and supine positions. RESULTS: Upright plasma NE and ANP were significantly elevated in the patients compared with the controls (4.4 +/- 0.4 vs 2.1 +/- 0.2 nmol/l (p < 0.001) and 1.3.5 +/- 2.1 vs 6.9 +/- 1.0 nmol/l (p < 0.01) respectively). With change from upright to supine position plasma NE decreased in the controls (2.2 +/- 0.3 vs 1.7 +/- 0.3 nmol/l) (p < 0.01) and patients (3.8 +/- 0.4 vs 2.6 +/- 0.4) (p < 0.01). Supine ANP increased in controls (5.5 +/- 1.0 vs 8.3 +/- 1.1) (p < 0.01) but not in patients (14.3 +/- 3.8 vs 16.1 +/- 3.8 nmol/l) (p > 0.10). Plasma NE correlated positively with MAP (p < 0.001) and negatively with GFR (p < 0.01) in the upright but not supine position. A positive correlation between NE and ANP was observed in upright (p < 0.001) but not in supine position. ANP correlated negatively with GFR in the upright (p < 0.01) but not supine position. No position dependent changes were seen in GFR and ERPF, but supine filtration fraction (FF) increased insignificantly in the patient group (0.23 +/- 0.02 vs 0.24 +/- 0.02) (p < 0.05). CONCLUSION: Hypertensive patients with reduced GFR have elevated levels of plasma NE and ANP in the upright body position. When the upright and supine positions are compared, plasma NE declines in the supine position in controls and hypertensive renal failure patients. and plasma ANP levels are elevated only in the upright position in hypertensive renal failure patients where the sympathetic nervous system is activated. A significant positive relationship between plasma NE and ANP was observed only in the upright position. The upright body position seems superior to recumbency in the characterization of these hormonal changes in hypertensive chronic renal failure patients.

Atrial Natriuretic Factor↗
PubMed2006

Hand-held monitor of sympathetic nervous system using salivary amylase activity and its validation by driver fatigue assessment.

In order to realize a hand-held monitor of the sympathetic nervous system, we fabricated a completely automated analytical system for salivary amylase activity using a dry-chemistry system. This was made possible by the fabrication of a disposable test-strip equipped with built-in collecting and reagent papers and an automatic saliva transfer device. In order to cancel out the effects of variations in environmental temperature and pH of saliva, temperature- and pH-adjusted equations were experimentally determined, and each theoretical value was input into the memory of the hand-held monitor. Within a range of salivary amylase activity between 10 and 140 kU/l, the calibration curve for the hand-held monitor showed a coefficient with R(2)=0.97. Accordingly, it was demonstrated that the hand-held monitor enabled a user to automatically measure the salivary amylase activity with high accuracy with only 30 microl sample of saliva within a minute from collection to completion of the measurement. In order to make individual variations of salivary amylase activity negligible during driver fatigue assessment, a normalized equation was proposed. The normalized salivary amylase activity correlated with the mental and physical fatigue states. Thus, this study demonstrated that an excellent hand-held monitor with an algorithm for normalization of individuals' differences in salivary amylase activity, which could be easily and quickly used for evaluating the activity of the sympathetic nervous system at any time. Furthermore, it is suggested that the salivary amylase activity might be used as a better index for psychological research.

Adult↗
PubMed1997

Thyroid hormone stimulates renin synthesis in rats without involving the sympathetic nervous system.

The present study was performed to examine whether renal expression of the renin gene is regulated by thyroid hormone. Thirty male Sprague-Dawley rats were divided into hypothyroid, control, and hyperthyroid groups by use of daily intraperitoneal administration of methimazole, saline vehicle, or thyroxine, respectively. Each group was further subdivided into sympathetic innervated and sympathetic denervated subgroups by use of intraperitoneal administration of saline vehicle or 6-hydroxydopamine. Plasma renin activity and renal levels of renin were measured by radioimmunoassays after 8 wk. Renal expression of renin mRNA was evaluated by a semiquantitative reverse transcriptase-polymerase chain reaction. Compared with control animals, plasma renin activity, renal level of renin, and renal expression of renin mRNA were reduced (82, 94, and 71%, respectively) in hypothyroid animals and elevated (155, 1,182, and 152%, respectively) in hyperthyroid animals. Sympathetic denervation had no independent effect on these renin values. Our results indicate that thyroid hormone stimulates renin synthesis without involving the sympathetic nervous system.

Animals↗
PubMed2001

Regulation of sympathetic nervous system function after cardiovascular deconditioning.

Humans subjected to prolonged periods of bed rest or microgravity undergo deconditioning of the cardiovascular system, characterized by resting tachycardia, reduced exercise capability, and a predisposition for orthostatic intolerance. These changes in cardiovascular function are likely due to a combination of factors, including changes in control of body fluid balance or cardiac alterations resulting in inadequate maintenance of stroke volume, altered arterial or venous vascular function, reduced activation of cardiovascular hormones, and diminished autonomic reflex function. There is evidence indicating a role for each of these mechanisms. Diminished reflex activation of the sympathetic nervous system and subsequent vasoconstriction appear to play an important role. Studies utilizing the hindlimb-unloaded (HU) rat, an animal model of deconditioning, evaluated the potential role of altered arterial baroreflex control of the sympathetic nervous system. These studies indicate that HU results in blunted baroreflex-mediated activation of both renal and lumbar sympathetic nerve activity in response to a hypotensive stimulus. HU rats are less able to maintain arterial pressure during hemorrhage, suggesting that diminished ability to increase sympathetic activity has functional consequences for the animal. Reflex control of vasopressin secretion appears to be enhanced following HU. Blunted baroreflex-mediated sympathoexcitation appears to involve altered central nervous system function. Baroreceptor afferent activity in response to changes in arterial pressure is unaltered in HU rats. However, increases in efferent sympathetic nerve activity for a given decrease in afferent input are blunted after HU. This altered central nervous system processing of baroreceptor inputs appears to involve an effect at the rostral ventrolateral medulla (RVLM). Specifically, it appears that tonic GABAA-mediated inhibition of the RVLM is enhanced after HU. Augmented inhibition apparently arises from sources other than the caudal ventrolateral medulla. If similar alterations in control of the sympathetic nervous system occur in humans in response to cardiovascular deconditioning, it is likely that they play an important role in the observed tendency for orthostatic intolerance. Combined with potential changes in vascular function, cardiac function, and hypovolemia, the predisposition for orthostatic intolerance following cardiovascular deconditioning would be markedly enhanced by blunted ability to reflexly activate the sympathetic nervous system.

Animals↗
PubMed2002

Influence of ageing on the sympathetic nervous system and adrenal medulla at rest and during stress.

The influence of ageing on the sympathetic nervous system and adrenal medulla was studied neurochemically in humans, using isotopic dilution measurement of regional and whole body catecholamine release to plasma in humans. With ageing, sympathetic activation was evident in the heart, and the gut and liver at rest. The mechanism appeared to be by activation of sympathoexcitatory noradrenergic suprabulbar projections from the brainstem. Sympathetic nervous responses with stressors were augmented. Conversely, adrenal medullary release of epinephrine was subnormal in the elderly, at rest and during stress.

Adrenal Medulla↗
PubMed1988

Persistent sympathetic nervous system arousal associated with tethering in cynomolgus macaques.

The swivel-tether system has been used extensively in biomedical research involving nonhuman primates, yet there has been little or no investigation into potential adverse influences of this form of restraint on research results. In the study described here, a portable electrocardiographic telemetry system was used for continuous monitoring of the heart rate of 26 cynomolgus monkeys while: (a) pair-caged, 8 weeks prior to tethering; (b) singly-caged, tethered; (c) singly-caged, tethered, administered propranolol (30 mg/kg/day) in the diet; (d) group-housed (five monkeys per group), 1 week after group formation; and (e) group-housed (five monkeys per group), 4 weeks after group formation. Tethering resulted in persistent elevations in heart rate relative to the other conditions. Administration of propranolol, a beta-adrenergic antagonist, resulted in an abrupt, sustained decrease in heart rate indicating that the increase in heart rate associated with tethering was due to persistent stimulation of the sympathetic nervous system. Since multiple aspects of cardiovascular function are influenced by the sympathetic nervous system, and other organs and systems (e.g., pituitary-gonadal) also may be affected, investigators using the swivel-tether system should be cognizant of these potential effects when designing experiments and interpreting the results.

Analysis of Variance↗
PubMed2005

Physical activity and stress resistance: sympathetic nervous system adaptations prevent stress-induced immunosuppression.

A physically active lifestyle incurs many health benefits. One recently recognized benefit of regular moderate exercise is stress reduction. The current review develops the hypothesis that physical activity may prevent stress-induced suppression of the immune system and suggests an immunophysiological mechanism (sympathetic nervous system constraint) for this effect.

Adaptation, Physiological↗
PubMed1982

Decrease in sympathetic nervous system activity and attenuation in response to stress following renal denervation in the one-kidney one-clip Goldblatt hypertensive rat.

We have found that renal denervation in the one-kidney one-clip Goldblatt hypertensive rat results in an attenuation of the hypertension associated with a decrease in sympathetic nervous system activity. To test further the hypothesis that the renal nerves (afferents) contribute to the maintenance of hypertension in this model by modulating sympathetic nervous system activity, plasma norepinephrine and epinephrine changes in response to stress were compared in hypertensive sham-operated (n = 6), renal denervated (n = 6) and control (n = 7) animals. Stress was produced in conscious resting unrestrained animals by administering two brief electrical stimulations to the hindlimb. Resting plasma norepinephrine was significantly higher (P less than 0.01) in hypertensive sham-operated (420 +/- 41 pg/ml) compared to renal denervated (289 +/- 23 pg/ml) or control (296 +/- 25 pg/ml) animals. There was no difference in resting plasma epinephrine among the groups. In response to stress there were significantly greater absolute increases in plasma norepinephrine and epinephrine in hypertensive sham-operated animals compared to renal denervated and control groups, suggesting that the one-kidney one-clip rat exhibits an enhanced sympathoadrenal response to stress. The response to stress in renal denervated rats was the same as that in the control group. Taken together, these data support the concept that the renal afferent nerves modulate sympathetic nervous system activity in the one-kidney one-clip hypertensive rat.

Animals↗
PubMed1994

Sympathetic nervous system activity in major depression. Basal and desipramine-induced alterations in plasma norepinephrine kinetics.

BACKGROUND: To determine whether elevations of plasma norepinephrine (NE) in major depression represent increased sympathetic nervous system (SNS) activity and to assess the effects of desipramine hydrochloride on sympathetic function. METHODS: SNS activity was assessed in depressed patients and controls by an isotope-dilution, plasma NE kinetic technique using mathematical modeling and compartmental analysis. This approach provided estimates of the rate of NE appearance into an extravascular compartment, which is the site of endogenous NE release from SNS nerves, the corresponding rate of NE appearance into plasma, and the rate of NE clearance from plasma. RESULTS: Norepinephrine appearance into the extravascular and vascular compartments was significantly elevated in 17 depressed patients compared with that in 36 controls. The rate of NE clearance from plasma was similar in both groups. This is compatible with increased SNS activity in major depression. Desipramine, given for 2 days, significantly reduced the concentration of NE in plasma of patients and controls by markedly suppressing the rates of extravascular and vascular NE appearance, compatible with a short-term reduction in SNS activity. Desipramine prolonged the rate of NE clearance from plasma, consistent with a blockade of NE re-uptake into SNS nerve terminals. The initial suppression of SNS activity by desipramine was reversed by long-term (28 days) treatment of patients, with extravascular and vascular NE appearance rates returning to approximately basal levels. An associated rise in plasma NE concentrations compared with the baseline was attributable to a progressive reduction in plasma NE clearance. CONCLUSION: Sympathetic nervous system activity is elevated in major depression and is suppressed by short-term desipramine administration. The demonstration of SNS reactivation occurring with prolonged desipramine treatment is compatible with the theory that long-term treatment desensitizes CNS alpha 2-adrenergic receptors and emphasizes the value of examining the temporal course of responses to pharmacological challenges of neuroendocrine systems. Previously reported elevations of plasma NE during prolonged administration of tricyclic antidepressants are probably the result of a reduction in plasma NE clearance, not an increase in SNS activity.

Adult↗
PubMed1995

Suppression of sympathetic nervous system is involved in hypotension and bradycardia during hemofiltration in anesthetized dogs.

Hypotension occurring during hemodialysis is often accompanied by paradoxical bradycardia. However, the mechanism is poorly understood. This study was designed to determine the role of the sympathetic nervous system in hemodialysis-induced hypotension and bradycardia. We measured efferent sympathetic nerve activities to the heart (CNA), kidney (RNA), liver (HNA), spleen (SpNA), and adrenal gland (AdNA), along with heart rate (HR), blood pressure (BP), central venous pressure (CVP), and left atrial pressure (LAP) during hemofiltration performed at a rate of 0.3 mL .center dot Kg(-1) center dot min(-1) for 30 min in anesthetized dogs. The response to hemorrhage was also studied at the same bleeding speed. Hemorrhage caused a decrease in BP (-18 +/- 1 mmHg; 1 mmHg = 133.3 Pa) with reflex increases in HR (7 +/- 2 beats/min) and sympathetic nerve activities. In contrast, hemofiltration caused a decrease in CNA (85 +/- 18%), HNA (86 +/- 11%), and SpNA (88 +/- 11%) with greater decreases in BP (-43 +/- 10 mmHg) and HR (-27 +/- 14 beats/min) than hemorrhage. During hemofiltration, the decreases in BP, HR, CNA, HNA, and SpNA were attenuated after vagotomy. Hematocrit increased by 6.5% at 30 min after hemofiltration, whereas it decreased by 4.3% after hemorrhage. These results suggest that hemofiltration suppresses the sympathetic nervous system, resulting in decreases in HR and BP. Furthermore, this sympathetic suppression during hemofiltration is mediated by vagal afferents.

Animals↗
PubMed1970

An assessment of the role of the sympathetic nervous system in experimental hypertension using normal and immunosympathectomized rats.

1. The role of the sympathetic nervous system in experimental hypertension and associated changes in aortic sodium and potassium was studied using normal and immunosympathectomized Sprague-Dawley rats.2. A single injection of antiserum to nerve-growth factor to rats at birth produced less intensive destruction of the peripheral sympathetic system than did two injections (one daily for 2 days). The former are referred to as "partial" immunosympathectomized and the latter as "total" immunosympathectomized rats.3. Maintenance of rats on 1% sodium chloride after unilateral nephrectomy and implantation of 40 mg desoxycorticosterone acetate (DOCA) pellets resulted in sustained DOCA-NaCl hypertension in both normal and "partial" immunosympathectomized rats but not in "total" immunosympathectomized rats. Hypertension was associated with an increase in aortic sodium.4. Constriction of one renal artery with contralateral nephrectomy caused sustained hypertension and an increase in aortic sodium in normal and "partial" immunosympathectomized rats. Renal hypertension in "total" immunosympathectomized rats was not sustained.5. It is concluded that a certain minimum control of the cardiovascular system by the sympathetic system is essential for the production of experimental hypertension and associated electrolyte changes.

Animals↗