Sympathetic Nervous Regulation Research Articles

Modified Sympathetic Nerve System Activity with Overexpression of the Voltage-dependent Calcium Channel β3 Subunit

N-type voltage-dependent calcium channels (VDCCs) play determining roles in calcium entry at sympathetic nerve terminals and trigger the release of the neurotransmitter norepinephrine. The accessory beta3 subunit of these channels preferentially forms N-type channels with a pore-forming CaV2.2 subunit. To examine its role in sympathetic nerve regulation, we established a beta3-overexpressing transgenic (beta3-Tg) mouse line. In these mice, we analyzed cardiovascular functions such as electrocardiography, blood pressure, echocardiography, and isovolumic contraction of the left ventricle with a Langendorff apparatus. Furthermore, we compared the cardiac function with that of beta3-null and CaV2.2 (alpha1B)-null mice. The beta3-Tg mice showed increased expression of the beta3 subunit, resulting in increased amounts of CaV2.2 in supracervical ganglion (SCG) neurons. The beta3-Tg mice had increased heart rate and enhanced sensitivity to N-type channel-specific blockers in electrocardiography, blood pressure, and echocardiography. In contrast, cardiac atria of the beta3-Tg mice revealed normal contractility to isoproterenol. Furthermore, their cardiac myocytes showed normal calcium channel currents, indicating unchanged calcium influx through VDCCs. Langendorff heart perfusion analysis revealed enhanced sensitivity to electric field stimulation in the beta3-Tg mice, whereas beta3-null and Cav2.2-null showed decreased responsiveness. The plasma epinephrine and norepinephrine levels in the beta3-Tg mice were significantly increased in the basal state, indicating enhanced sympathetic tone. Electrophysiological analysis in SCG neurons of beta3-Tg mice revealed increased calcium channel currents, especially N- and L-type currents. These results identify a determining role for the beta3 subunit in the N-type channel population in SCG and a major role in sympathetic nerve regulation.

Regulation of sympathetic nerve traffic to skeletal muscle in resting humans

An overview is given of microneurographic studies of resting vasoconstrictor traffic in human muscle nerves (muscle sympathetic nerve activity = MSNA). In multiunit recordings, the activity consists of synchronized bursts of vasoconstrictor impulses, the outflow of which is under potent arterial baroreflex control. In agreement with this, the bursts always display cardiac rhythmicity and occur during temporary reductions of blood pressure. Burst occurrence shows a close inverse correlation to variations of diastolic blood pressure whereas the correlation to the strength of the bursts is weak or absent, suggesting that the mechanisms controlling the two parameters are not identical. These dynamic characteristics are similar in all subjects despite large, reproducible, interindividual differences in number of bursts. Such interindividual differences probably have a genetic origin, and since discharge frequencies in single vasoconstrictor fibers are similar in subjects with few and many bursts, the differences in multiunit activity are likely to be due to a higher number of active fibers in subjects with many bursts. The interindividual differences in multiunit activity are not associated with differences in resting blood pressure levels. Recent studies have revealed (a) an inverse relationship between resting levels of cardiac output and MSNA and (b) evidence of reduced vascular responsiveness to noradrenaline in subject with many sympathetic bursts at rest. These findings suggest that the vasoconstriction induced by the sympathetic impulses is balanced or reduced by these factors, which thereby contribute to the poor relationship between the mean number of sympathetic bursts and the blood pressure level.

Malfunction of Vascular Control in Lifestyle-Related Diseases: Oxidative Stress of Angiotensin II-induced Hypertension: Mitogen-Activated Protein Kinases and Blood Pressure Regulation

The candidate mechanisms for maintaining hypertension in a chronically angiotensin II (Ang II)-infused state include direct vasoconstriction of the vasculature, disturbance of renal water/sodium handling, and central/peripheral sympathetic nerve regulation of hemodynamics. The involvement of reactive oxygen species (ROS) has been studied in these proposed mechanisms and the importance of ROS in progression of Ang II-induced hypertension has been accepted. We recently reported ROS-sensitive blood pressure regulation in chronically as well as acutely Ang II-infused hypertensive rats. The facts suggested that mechanisms for maintaining high peripheral vascular resistance in chronically Ang II-infused hypertensive rats were different from those involved in the acute hypertensive response to Ang II from the perspective of ROS sensitivity and that there must be a time-dependent transition from ROS-non-sensitive to ROS-sensitive vasoconstriction during prolonged Ang II infusion. In this review, we introduced our recent work describing the time transition of ROS sensitivity in Ang II-induced hypertension and activation of cardiovascular mitogen-activated protein kinase (MAPK) in acute and chronic phases Ang II infusion in conscious rats.

Stimulation and blockade of GABA(A) receptors in the raphe pallidus: effects on body temperature, heart rate, and blood pressure in conscious rats.

Studies in anesthetized rats have implicated GABAA receptors in the region of the medullary raphe pallidus (RP) at the level of the facial nucleus in sympathetic nervous regulation of both heart rate and thermoregulatory mechanisms. Therefore, we examined the effect of microinjection of muscimol, a GABAA receptor agonist, and of bicuculline methiodide (BMI), a GABAA receptor antagonist, into the same region of the RP on heart rate, blood pressure, and core body temperature in conscious rats. Microinjection of BMI (40 pmol) into the RP evoked tachycardia that appeared within 1 min and was maximal within 10 min but had little or no effect on blood pressure or body temperature. Microinjection of muscimol (10-80 pmol) at the same sites in the RP evoked marked dose-related decreases in body temperature that developed more slowly (i.e., maximum decreases appearing at 60-75 min after 80 pmol) but had no effect on heart rate or blood pressure. Injection of either agent at sites outside the region had lesser or no effect on the measured parameters. These findings suggest that activity of neurons in the region of the RP plays an important role in the maintenance of body temperature but not heart rate under baseline conditions in conscious rats. Specifically, thermoregulatory neurons in this region appear to be tonically active and contribute to maintenance of body temperature under baseline conditions, while cardiac sympathetic premotor neurons in the RP are not active under these circumstances and thus do not support basal heart rate in conscious rats.

Sympathetic nerve regulation to heating is altered in senescent rats.

Renal and splanchnic sympathetic nerve discharge (SND) responses to increased (38-41 degrees C) internal temperature were determined in anesthetized young (3-6 mo old), mature (12 mo old), and senescent (24 mo old) Fischer 344 (F344) rats. We hypothesized that SND responses would be altered in senescent and mature rats as demonstrated by attenuated sympathoexcitatory responses to heating and by the absence of hyperthermia-induced SND pattern changes. The following observations were made. 1) Renal and splanchnic SND responses were significantly increased during heating in young and mature but not in senescent rats. 2) At 41 degrees C, renal and splanchnic SND responses were higher in young compared with senescent rats, and renal SND was higher in mature than in senescent rats. 3) Heating changed the SND bursting pattern in young, but not in mature or senescent, rats. 4) SND responses to heating did not differ between baroreceptor-innervated (BRI) and sinoaortic-denervated (SAD) senescent rats but were higher in SAD compared with BRI young rats. These results demonstrate an attenuated responsiveness of sympathetic neural circuits to heating in senescent F344 rats.

Renal sympathetic nerve regulation to heating is altered in rats with heart failure

Heart failure (HF) alters the regulation of basal sympathetic nerve discharge (SND); however, the effect of HF on SND responses to acute stress is not well established. In the present study, renal SND responses to hyperthermia were determined in chloralose-anesthetized HF rats and in sham controls. Whole body heating (colonic temperature increased from 38 to 41 degrees C) was used as an acute stressor because increased internal body temperature provides a potent stimulus to the sympathetic nervous system. Left ventricular end-diastolic pressure and the right ventricular wt-to-body wt ratio were increased (P < 0.05) in HF compared with sham rats. The following observations were made: 1) renal sympathoexcitatory responses to heating were significantly reduced in HF compared with sham rats, 2) renal blood flow remained unchanged from control levels during heating in HF rats but was significantly reduced in sham rats, and 3) renal SND responses to heating were significantly higher in HF rats with bilateral lesions of the hypothalamic paraventricular nucleus (PVN) compared with sham PVN-lesioned HF rats. These results demonstrate a marked attenuation in the responsiveness of renal SND to heating in HF rats and suggest that HF alters the organization of neural pathways mediating SND responses to heating.

Blockade of central angiotensin II does not affect the reduction in renal sympathetic nerve activity following a volume load in heart failure rabbits.

1. We investigated the role in sympathetic nerve regulation of endogenous angiotensin (Ang)II in the brain in heart failure by examining the effect of losartan on the resting mean arterial blood pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) and the reflex reduction in RSNA elicited by acute volume expansion in conscious rabbits. 2. Heart failure was induced with doxorubicin (1 mg/kg, i.v., twice weekly for 6 weeks). On the experimental day, MAP, HR and RSNA were recorded in conscious rabbits before and after losartan (10 microg; n = 6) or Ringer's (control; n = 5) injected in the fourth brain ventricle. Animals were then administered an acute volume load with the plasma expander Haemaccel (Hoechst Marion Roussel, Lane Cove, NSW, Australia; 2 mL/min, i.v., for 30 min). 3. Losartan did not significantly affect the resting basal levels of MAP, HR and RSNA. There was no significant difference between losartan- and Ringer's-treated animals. 4. Volume expansion in the control group elicited a significant reduction of 40% in RSNA. In the losartan-treated group, a similar reduction (42%) was observed. There was no significant difference between the treatments. The administration of losartan did not significantly affect MAP and HR during volume expansion compared with the control group. 5. We conclude that AngII in the brainstem does not play a major role in the maintenance of resting MAP, HR and RSNA or in the reflex reduction in RSNA elicited by volume expansion in the conscious rabbit with doxorubicin-induced heart failure.

Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans.

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an alpha adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (delta CBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after alpha blockade, after alpha and beta blockade, and after alpha and beta blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, delta CBF decrease and delta CBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between delta CBF and BPS were significant before inhibition and after inhibition of ANS. For BPS below 160 mmHg, BPS and delta CBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate: even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Neurotransmitters involved in the central regulation of the cardiovascular system.

Arterial blood pressure is maintained by the tonic vasomotor activity of sympathetic preganglionic neurons which are located in the intermediolateral cell column of the thoracic and lumbar spinal cord. Supraspinal inputs are critical in maintaining the activity of SPN. The medulla and pons have been recognized as essential for maintaining tonic sympathetic activity since the late 1800’s when experiments showed that transection of the brain stem caudal to the inferior colliculus failed to lower blood pressure. Transections more caudally produced increasingly greater falls in blood pressure. Reductions in blood pressure reached a maximum with transections at the level of the obex (see ref [1] for historical review). A major goal of central autonomic research has been to identify the descending neuronal pathways which project to SPN and to determine the neurotransmitters contained within these pathways (see ref [2–6] for review). Neuroanatomical and immunocytochemical techniques have been used to identify chemically specific pathways between areas thought to be important in central autonomic regulation. This information combined with experiments utilizing sophisticated electrophysiological and pharmacological analysis have begun to elucidate the role of these pathways in central autonomic regulation and to determine the functional significance of putative neurotransmitters contained within these pathways. This review describes recent developments which have had a major influence on our understanding of the central neurotransmitters involved in the regulation of sympathetic nerve discharge.KeywordsNucleus Tractus SolitariusVentrolateral MedullaRostral Ventromedial MedullaNucleus AmbiguusPreganglionic NeuronThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Sympathetic nervous regulation of retinal blood flow in aged rats

Sympathetic nervous regulation of retinal blood flow in aged rats

Altered sympathetic control of nutrient mobilization during physical exercise after lesions in the VMH

To study the impact of obesity on sympathetic nervous regulation of nutrient mobilization, obese rats and lean controls were subjected to physical exercise. Male Wistar rats, rendered obese by bilateral electrolytic lesions of the ventromedial hypothalamus (VMH) were subjected to 15 min swimming. Permanent cardiac catheters allowed frequent blood sampling. At rest, glucose, free fatty acids (FFA), and insulin concentrations were elevated in the obese animals, whereas catecholamine levels were similar in both groups. During exercise, glucose concentrations reached higher values in the lesioned rats, whereas these animals did not display the normal FFA increment. Plasma insulin concentrations were suppressed in both groups, and the rate of suppression was very similar when expressed as percentage change from resting levels. There was no difference in plasma epinephrine responses during swimming, but the increase in norepinephrine was diminished in the obese animals. The results suggest that obesity after VMH lesion leads to reduced stimulation of lipolysis by norepinephrine and a predominant mobilization of glucose during exercise, both favoring glucose utilization and the accumulation of fat.

Sympathetic Nervous Regulation in Patients with Cirrhosis: Pathogenesis of Fluid Retention and Formation of Ascites

Increased circulating noradrenaline in patients with cirrhosis is due to enhanced sympathetic nervous activity and is not merely the result of decreased clearance of catecholamines. There is a direct relation between the level of arterial norndrenaline and severity of cirrhosis, increased portal pressure and fluid accumulation; patients with the hepatorenal syndrome exhibit the highest values of plasma noradrenaline. In patients with cirrhosis, the kidneys have been identified as an important source of noradrenaline ‘spillover’ into plasma, which indicates enhanced sympathetic nervous activity in these organs. Moreover, the level of plasma noradrenaline is inversely related to renal bloodflow and urinary excretion of sodium, and directly related to plasma renin, vasopressin and aldosterone. An increased spillover of noradrenaline has recently been demonstrated in the splanchnic system and superior portosystemic collaterals. Reduced central and arterial blood volume and low arterial blood pressure secondary to peripheral vasodilation are probably important afferent stimuli for enhanced sympathetic nervous activity, although a nonvolume-dependent hepatic baroreceptor may also be present. The authors conclude that the sympathetic nervous system, in concert with other regulatory systems, plays an important role in sodium-water homeostasis and fluid retention, as well as in the systemic and hepatosplanchnic circulatory derangement seen in patients with cirrhosis.

Participation of the parasympathetic and sympathetic nerves in regulation of gallbladder motility in the dog.

The participation of the parasympathetic and sympathetic nerves in the canine gallbladder motility was examined. Efferent stimulation of the parasympathetic (vagus) and sympathetic (celiac) nerves caused contraction or inhibition of the neck, body and fundus of the gallbladder. The contractile response induced by vagus nerve stimulation was reduced by subthreshold efferent stimulation of the celiac nerve, while the inhibitory response was neither reduced nor enhanced by subthreshold efferent stimulation of the celiac nerve. The contractile and inhibitory response induced by celiac nerve stimulation was not reduced in the neck, body and fundus by subthreshold efferent stimulation of the vagus nerve. The contractile response to vagus nerve stimulation was reversed to a relaxant response by atropine administration, which was reduced or abolished by hexamethonium. It is suggested that the vagus nerve-induced contractile response in the canine gallbladder is modulated by sympathetic nerves presynaptically at the vagus nerve endings in the enteric ganglion, but the vagus nerve-induced relaxant response, which probably was induced by non-adrenergic non-cholinergic inhibitory neurons, is not modulated by the sympathetic nerves.

Cervical preganglionic sympathetic nerve activity and chemoreflexes in the cat

The role of chemoreflexes originating from carotid body and central chemoreceptors in the regulation of cervical preganglionic sympathetic nerve (PSN) activity was studied in anesthetized and spontaneously breathing cats. PSN efferents which responded to hypoxia were selected for the study. The PSN activity, breath-by-breath inspiratory tidal volume, tracheal PO2 and PCO2, and arterial systemic blood pressure were recorded simultaneously. The responses of PSN efferents to transient changes in and steady-state levels of arterial PO2 and PCO2 and to graded bolus injections of intravenous sodium cyanide (50-100 micrograms), nicotine (50-100 micrograms), and dopamine hydrochloride (30-60 micrograms) were compared before and after bilateral section of carotid sinus nerves (CSN). CSN section raised the base-line PSN activity and practically eliminated the responses to brief pharmacological stimuli, but it did not eliminate the responses to transient changes in and steady-state levels of arterial PO2 and PCO2. However, CSN section diminished PSN responses and abolished ventilatory responses to hypoxia. Thus the PSN response to hypoxia was partly independent of peripheral chemoreflex and of respiratory drive. We conclude that carotid body chemoreflex elicits fast PSN responses and that a moderate decline in arterial PO2 causes an additional slow, direct excitation of sympathetic nervous system. The latter indicates O2 chemosensitivity of the system in the physiological range of arterial PO2. This O2-sensing property may allow sympathetic nervous system to initiate chemoreflex responses independent of the peripheral chemoreceptors.

Neuromuscular dysfunction of the lower urinary tract with special reference to the influence of the sympathetic nervous system.

Filling cystometry, urethral and anal sphincter electromyography, pressure-flow registration, urethral closure pressure profile at rest and after alpha-adrenoceptor blockade with phentolamine, evoked potential of the bulbocavernosus reflex and denervation supersensitivity to carbachol in a-reflexic bladders were performed in 57 consecutive patients with a localized neurological lesion, in order to evaluate the relative importance of the somatic, the parasympathetic and especially the sympathetic nervous system for the function of the lower urinary tract. In spinal lesions with detrusor hyperreflexia, dyscoordination between detrusor and striated urethral sphincter was dominant, while in cauda equina lesions and in lesions of the pelvic nerves the lack of parasympathetic bladder innervation dominated. It was not possible to identify specific spinal segments controlling sympathetic nervous regulation of the lower urinary tract. The only influence of the sympathetic nervous system was a control of urethral pressure, where a statistically significant smaller proportion of the maximal urethral pressure was affected after alpha-adrenergic blockade in patients with peripheral nerve lesions. All a-reflexic bladders exhibited denervation supersensitivity to carbachol, while carbachol did not change urethral pressure significantly indicating minimal influence of the parasympathetic nervous system on urethral pressure.

Tissue gases during hypovolemic shock.

ArticleTissue gases during hypovolemic shock.J W Brantigan, E C Ziegler, K M Hynes, T Y Miyazawa, and A M SmithJ W Brantigan, E C Ziegler, K M Hynes, T Y Miyazawa, and A M SmithPublished Online:01 Jul 1974https://doi.org/10.1152/jappl.1974.37.1.117MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats21 March 2016 | PLOS ONE, Vol. 11, No. 3Diaphragmatic Function Is Preserved during Severe Hemorrhagic Shock in the RatAnesthesiology, Vol. 120, No. 2A Review of the Clinical Significance of Tissue Hypoxia Measurements in Lower Extremity Wound Management29 June 2016 | The International Journal of Lower Extremity Wounds, Vol. 6, No. 4TRANSCUTANEOUS PRESSURE OF OXYGENShock, Vol. 26, No. 5EARLY DIFFERENCE IN TISSUE PH AND MICROVASCULAR HEMODYNAMICS IN HEMORRHAGIC SHOCK RESUSCITATION USING POLYETHYLENE GLYCOL-ALBUMIN- AND HYDROXYETHYL STARCH-BASED PLASMA EXPANDERSShock, Vol. 24, No. 1End points of resuscitation: Choosing the right parameters to monitorDimensions of Critical Care Nursing, Vol. 21, No. 1Skeletal Muscle Acidosis Correlates with the Severity of Blood Volume Loss during Shock and ResuscitationJournal of Trauma and Acute Care Surgery, Vol. 51, No. 6Endpoints of Resuscitation for the Victim of TraumaJournal of Intensive Care Medicine, Vol. 16, No. 2Effects of hyper- and hypoventilation on gastric and sublingual PCO2Andrej Pernat, Max Harry Weil, Wanchun Tang, Hitoshi Yamaguchi, Andreja Marn Pernat, Shijie Sun, and Joe Bisera1 September 1999 | Journal of Applied Physiology, Vol. 87, No. 3Comparison of skeletal muscle PO2, PCO2, and pH with gastric tonometric PCO2 and pH in hemorrhagic shockCritical Care Medicine, Vol. 27, No. 9Skeletal Muscle PO sub 2, PCO sub 2, and pH in Hemorrhage, Shock, and Resuscitation in DogsThe Journal of Trauma: Injury, Infection, and Critical Care, Vol. 44, No. 1Measurement of venous oxyhaemoglobin saturation in the adult human forearm by near infrared spectroscopy with venous occlusionMedical & Biological Engineering & Computing, Vol. 35, No. 4Subcutaneous and Splanchnic Tissue Perfusion During Hypovolemia Evaluated by Tissue Gases and Ph MeasurementsSubcutaneous Tissue Oxygen PressureThe Journal of Trauma: Injury, Infection, and Critical Care, Vol. 40, No. SupplementTranscutaneous OxymetryIntraarterial Perfusion of the Hindlimb with Pyridoxalated Hemoglobin Polyoxyethylene Conjugate Solution in Anesthetized DogsArtificial Organs, Vol. 19, No. 6Subcutaneous oxygen tensionCritical Care Medicine, Vol. 23, No. 5Continuous Tissue Oxygenation Assessment During Bloodflow Alterations in an Isolated Hindlimb Model of the PigSkeletal Muscle PO2 Assessment in ShockAssessment of perfusion in postoperative patients using tissue oxygen measurementsBritish Journal of Surgery, Vol. 74, No. 4Effects of haemorrhage on wound strength and fibroblast functionBritish Journal of Surgery, Vol. 74, No. 4Mass Spectrometry in the ICUMicrocirculation and hemorrhagic shockThe American Journal of Emergency Medicine, Vol. 2, No. 1Transcutaneous oxymetry measurements during acute blood lossAnnals of Emergency Medicine, Vol. 11, No. 10Continuous In Vivo Measurement of Gas Tension in Blood and in TissuesIntraoperative recording of tissue gas tensions in calf muscles of patients with peripheral arterial diseaseJournal of Surgical Research, Vol. 29, No. 6Physiological effects of increased tissue pressureInternational Orthopaedics, Vol. 3, No. 3Pathophysiology of ShockPathology - 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Clinical Observations on the Atrial Fibrillation, Paroxysmal Tachycardia and W.P.W. Syndrome with Special Reference to the Pathogenetic Mechanism of the Lone Arrhythmia

The authors carried out clinical and statistical studies about 161 patients with atrial fibrillation, paroxysmal tachycardia and W.P.W. syndrome. All patients have been in-patient in Maekawa Clinic of Kyoto University Hospital from 1949 to 1958. The exact mechanism of production of these arrhythmias is not clear ; theories have ascribed the main factor responsible for the arrhythmia of non-cardiac orignin to the unstable nervous system, to "vegetative Dystonie", or to autonomic disturbance, but there is little definite evidence against or for these theories. Especially, the authors studied clinically these lone or idiopathic arrhythmias from the point of view of the spinal sympathetic nervous regulation of the heart. And it may be concluded that pathogenetic origin of the lone arrhythmia is disturbance of spinal sympathetic control of the heart beat.