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PubMedDate not supplied

Are the sympathetic neural effects of digoxin and quinidine involved in their action on cardiac rhythm?

This study was initiated to determine if ventricular arrhythmia induced by digoxin was associated with a nonuniform neural discharge in the cardiac sympathetic postganglionic fibers. In addition, splanchnic neural discharge was monitored to explore the role of adrenal medullary catecholamines in digoxin-induced arrhythmia. Experiments were performed to ascertain whether the antiarrhythmic effects of quinidine in digoxin-induced arrhythmias were related to an action on cardiac sympathetic neural discharge induced by digoxin. All cats were anesthetized with alpha-chloralose and given atropine; some were pretreated with quinidine (10 or 20 mg/kg i.v. 15 min before digoxin). Digoxin was given every 15 min until death; the first three doses were 50 micrograms/kg i.v., and all subsequent doses were 25 micrograms/kg. The mean +/- SE time to arrhythmia was 32 +/- 4 min (n = 16) and was significantly increased only after 20 mg/kg quinidine (64 +/- 7 min; p less than 0.001). Mean +/- SE time to death was also increased from 74 +/- 4 to 98 +/- 7 min (p less than 0.001). Postganglionic cardiac sympathetic neural discharge before digoxin-induced arrhythmia was depressed. Of the 28 nerves monitored in 16 animals receiving digoxin, in the minute before development of arrhythmia, 22 nerves were depressed, 3 were increased, and 3 showed no change when compared with the predigoxin control. Following this depression of neural discharge, arrhythmia developed, and the neural discharge began to rise, eventually increasing above control levels. During this time the variability of the neural discharge increased greatly, as evidenced by large SE values, so that the mean values were not significantly different from control levels. Splanchnic neural discharge (n = 9) progressively decreased, reaching 66% of control values after the third injection of digoxin; the discharge then began to increase gradually toward control levels in the next 10 min and arrhythmia developed. The data indicate that the arrhythmias caused by digoxin are not associated with the development of nonuniform discharge patterns in the cardiac sympathetic nerves. Furthermore, action on the splanchnic nerve discharge is not involved in the arrhythmogenic effects of digoxin. Pretreatment with quinidine, 20 mg/kg, decreased both splanchnic and post-ganglionic cardiac sympathetic neural discharge, arterial blood pressure, and heart rate. Although quinidine, 20 mg/kg, increased the time to arrhythmia induced by digoxin, the depression of postganglionic cardiac or splanchnic neural discharge did not seem to be a major component of the antiarrhythmic effect of quinidine.

Animals↗

PubMed1960

Sympathetic postganglionic cholinergic fibres.

When the postganglionic fibres to the nictitating membrane are stimulated in a cat treated with reserpine, the membrane contracts. The contraction is increased after the injection of eserine and is abolished with atropine. Thus the fibres stimulated appear to be cholinergic. When the splenic nerve is stimulated in a cat treated with reserpine there is similar evidence of the presence of cholinergic fibres; the spleen dilates, the dilatation is greater in the presence of eserine and is abolished by atropine. The hypogastric nerves when stimulated cause inhibition of the uterus of the virgin cat. When the cat is treated with reserpine, stimulation then causes contraction which is increased in the presence of eserine and abolished by atropine. There is also evidence of cholinergic fibres in the postganglionic supply to the vessels of the rabbit's ear. From this and other evidence it is suggested that a form of adrenergic mechanism may exist such that cholinergic fibres in the postganglionic sympathetic supply liberate acetylcholine; this in turn liberates noradrenaline from a store around the sympathetic nerve ending.

Acetylcholine↗

PubMed1985

Local modulation of adrenergic neurotransmission in blood vessels.

Norepinephrine, released from sympathetic nerve terminals, has a key role in adjusting continuously the performance of the cardiovascular system. Although the amount of transmitter released depends primarily on the degree of activation of postganglionic sympathetic fibers, local metabolites and circulating vasoactive substances, in addition to affecting smooth-muscle cells directly, alter the amount of norepinephrine released. Thus, metabolic acidosis, an increase in potassium ions and in osmolality reduce the output of norepinephrine in the face of a constant frequency of stimulation of the postganglionic fibers. Many receptors have been identified on the prejunctional nerves which, when activated, can increase or decrease transmitter release. Those agonists which decrease it include adenosine and the adenine nucleotides, and norepinephrine, acetylcholine, histamine, and serotonin, acting on purinergic, alpha 2-adrenoceptors, muscarinic, H2-histaminergic and S1-serotoninergic receptors, respectively. Those that increase transmitter release include epinephrine (acting on beta 2-adrenoceptors) and angiotensin II. Part of the action of certain drugs is due to their prejunctional effects. Thus, cardiac glycosides cause a release of norepinephrine, and the antidepressant drug amitriptyline causes inhibition of prejunctional alpha-adrenoceptors and muscarinic receptors. Local changes in temperature also have complex actions on the neuroeffector junction and the vascular smooth muscle, which are of prime importance for cutaneous vessels.

Acetylcholine↗

PubMed1964

THE SYMPATHETIC POSTGANGLIONIC FIBRE AND THE BLOCK BY BRETYLIUM; THE BLOCK PREVENTED BY HEXAMETHONIUM AND IMITATED BY MECAMYLAMINE.

Acetylcholine, in the presence of atropine, has an action like that of sympathetic stimulation. When injected into the splenic artery it causes contraction of the spleen, but this action is blocked by hexamethonium; stimulation of the splenic nerves, however, is still effective. Thus hexamethonium distinguishes between sympathetic nerve stimulation and the action of acetylcholine. If bretylium is used instead of hexamethonium, there is no such distinction, for bretylium blocks the response to nerve stimulation as well as that to acetylcholine. It appeared that hexamethonium might block the action of acetylcholine by preventing its entry into the sympathetic fibre. Acetylcholine has some structural similarity to bretylium, since acetylcholine is a derivative of trimethylammonium and bretylium is a derivative of dimethylethylammonium. It has been found that hexamethonium, pentolinium and hemicholinium (HC-3), which are all bis-quaternary compounds, block the action of bretylium, presumably by preventing its entry into the fibre. Consistent with the view that ability to enter the fibre is important is the observation that mecamylamine and pempidine, which are ganglion-blocking agents, but not either mono- or bis-quaternary compounds, often abolish the response to stimulation of the sympathetic postganglionic fibre.

Acetylcholine↗

PubMed1996

Actions of Daiichi DQ-2511 on electrical and synaptic behavior of enteric neurons in the guinea-pig small intestine.

Intracellular recording of electrical and synaptic behavior of neurons in the enteric nervous system of guinea-pig small intestine was used to evaluate actions of DQ-2511 (3-[[[2-(3, 4-dimethoxyphenyl)ethyl]carbamoyl]methyl]amino-N-methylbenzamide). DQ-2511 is a new drug with gastrointestinal prokinetic action. DQ-2511 was most effective in the nanomolar range. The drug depolarized some of the neurons and this was accompanied by increased input resistance and augmented excitability. DQ-2511 in nanomolar concentrations increased the amplitude of fast excitatory postsynaptic potentials at nicotinic synapses. Slow inhibitory postsynaptic potentials, produced by release of norepinephrine from sympathetic postganglionic fibers, were suppressed by DQ-2511. This appeared to reflect presynaptic suppression of release of norepinephrine because postsynaptic responses to exogenously applied norepinephrine were unaffected. The results suggest that the prokinetic action of DQ-2511 on gastrointestinal transit might emerge from actions that augment excitatory synaptic transmission in the microcircuits of the enteric nervous system while suppressing inhibitory sympathetic neurotransmission.

Acetylcholine↗

PubMed1997

VIP -- a 'very important peptide' in the sympathetic nervous system?

Vasoactive intestinal peptide (VIP) is involved in the control of smooth muscle activity, blood flow and exo- as well as endocrine secretion. More recent work has elucidated the effects of this peptide on central and peripheral neurons. These studies suggest that VIP is an important modulator of cell growth, differentiation and neuronal survival during development of the sympathetic nervous system. VIP is also expressed in a subset of adult postganglionic sympathetic neurons. Furthermore, VIP is induced in an additional neuronal subpopulation of the rat superior cervical ganglion after axotomy. The mechanisms leading to increased VIP expression and its possible role during sympathetic nerve regeneration are currently being elucidated. This review summarizes the distribution, regulation and functions of VIP in cervical sympathetic ganglia of higher vertebrates.

Adrenergic Fibers↗

PubMed1999

Sympathetic neuronal oscillators are capable of dynamic synchronization.

In this paper we show that the discharges of sympathetic neurons innervating an identified peripheral target are driven by multiple oscillators that undergo dynamic synchronization when an entraining force, central respiratory drive (CRD), is increased. Activity was recorded from postganglionic sympathetic neurons (PGNs) innervating the caudal ventral artery of the rat tail: (1) at the population level from the ventral collector nerve (VCN); and (2) from pairs of single PGNs recorded simultaneously using a focal recording technique. Autospectral analysis of VCN activity revealed a more prominent rhythmical component in the presence of CRD than in its absence, suggesting that (1) multiple oscillators drive the discharges of PGNs and (2) these oscillators can be entrained and therefore synchronized by CRD. This interpretation was supported by analysis of the firing behavior of PGN pairs. Autocorrelation and cross-correlation analysis showed that pairs were not synchronized in the absence of CRD but showed significant synchronization when CRD was enhanced. Time-evolving spectral analysis and raster plots demonstrated that the temporal stability of PGN-to-PGN and CRD-to-PGN interactions at a given level of CRD were also dynamic in nature, with stable constant phase relationships predominating as CRD was increased. This is the first reported example of dynamic synchronization in populations of single postganglionic sympathetic neurons, and we suggest that, as in sensory processing and motor control, temporal pattern coding may also be an important feature of neuronal discharges in sympathetic pathways.

Animals↗

PubMed1990

[Histochemical and electron microscopic observation of the gastric wall after vagotomy].

Eight dogs underwent gastric total truncal vagotomy and another 8 had gastric superselective vagotomy. Specimens were take from anterior wall of gastric corpus and antrum at weeks after operation for histochemical and electron microscopic observation. The results showed: (1) the sympathetic postganglionic fibers in gastric wall were completely damaged. (2) response of gastric antrum mucosa to CCK-8 and gastric G-17 lowered markedly. (3) the amount of parietal cells increased, the structure of follicular atrophied, the number of mitochondrion in cytoplasm, and the stroma and micrailli on folilculi wall increased. (4) The Campylobacter-like organism (CLO) were found in mucosa of gastric antrum and corpus after operation. The authors discussed the role of gastric sympathetic nerve on gastric secretion and movement, and the relationship between CLO and ulcer recurrence after gastric superselective vagotomy.

Animals↗

PubMed1964

THE PART PLAYED BY CALCIUM IN DETERMINING THE RESPONSE TO STIMULATION OF SYMPATHETIC POSTGANGLIONIC FIBRES.

The inhibition of the pendular movements in a loop of rabbit ileum caused by stimulating the periarterial nerves in the mesentery depends on the calcium concentration in the bathing fluid. The inhibition is small when the concentration is low, and increases as the concentration rises. In the lower ranges of calcium concentration there is rarely any change in the response to noradrenaline, so that the increase in inhibition is due to an increase in the amount of noradrenaline released. The effect of calcium is antagonized by magnesium. In the presence of hyoscine, nicotine inhibits the ileum, and this inhibition also depends on the concentration of calcium. Acetylcholine can sometimes be shown to cause inhibition, and again this inhibition depends on the concentration of calcium. These and other experiments show a close similarity between the release of catechol amines from the adrenal medulla by acetylcholine and the release of noradrenaline from the postganglionic fibre by stimulation or by nicotine. In both instances the calcium concentration plays a decisive part.

Acetylcholine↗

PubMed1999

Augmented sympathetic activation during short-term hypoxia and high-altitude exposure in subjects susceptible to high-altitude pulmonary edema.

BACKGROUND: Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. METHODS AND RESULTS: We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to high-altitude pulmonary edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a high-altitude laboratory (4559 m). We also measured systolic pulmonary artery pressure to examine the relationship between sympathetic activation and pulmonary vasoconstriction. In subjects prone to pulmonary edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2- to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to edema (P<0.001). At high altitude, in subjects prone to edema, the increase in the mean+/-SE sympathetic firing rate was >2 times larger than in those resistant to edema (36+/-7 versus 15+/-4 bursts per minute, P<0.001) and preceded the development of lung edema. We observed a direct relationship between sympathetic nerve activity and pulmonary artery pressure measured at low and high altitude in the 2 groups (r=0.83, P<0.0001). CONCLUSIONS: With the use of direct measurements of postganglionic sympathetic nerve discharge, these data provide the first evidence for an exaggerated sympathetic activation in subjects prone to high-altitude pulmonary edema both during short-term hypoxic breathing at low altitude and during actual high-altitude exposure. Sympathetic overactivation may contribute to high-altitude pulmonary edema.

Adult↗

PubMed2001

The development of postganglionic sympathetic neurons: coordinating neuronal differentiation and diversification.

The fine-tuned operation of the nervous system is accomplished by a diverse set of neurons which differ in their morphology, biochemistry and, consequently, their functional properties. The accurate interconnection between different neuron populations and their target tissues is the prerequisite for physiologically appropriate information processing. This is exemplified by the regulatory action of the autonomic nervous system in vertebrates to sustain homeostasis under changing physiological demands. For this purpose, the coordination of divergent regulatory responses is required in a multitude of tissues spread over the entire body. To meet this task, diverse neuronal populations interact at different levels. In the sympathetic system. chemical relations between preganglionic and postganglionic neurons appear to differ along the rostrocaudal axis. In addition, postganglionic neurons innervating different target tissues at a segmental level have distinct properties. Differences in their preganglionic innervation and their integrative membrane properties result in diverse activation patterns upon reflex stimulation. Moreover, postganglionic neurons differ in the transmitter molecules they employ to convey information to the target tissues. The segregation of noradrenaline and acetylcholine to different populations of postganglionic sympathetic neurons is well established. A combination of cellular and molecular approaches has begun to uncover how such a complex system may be generated during development. Growth and transcription factors involved in noradrenergic and cholinergic differentiation are characterised. Interestingly, they can also promote the expression of proteins involved in transmitter secretion. As the proteins participating in the vesicle cycle are expressed in many neuron populations, whereas the enzymes of transmitter biosynthesis are restricted to subpopulations of neurons, the findings suggest that early in neuronal development subpopulation-specific and more widely expressed neuronal properties can be commonly induced. Still, many details concerning the signals involved in the induction of the neurotransmitter synthesis and release machinery remain to be worked out. Likewise, the regulatory processes resulting in differences of electrophysiological membrane properties and the specific recognition between pre- and postganglionic neurons have to be determined. Ultimately, this will lead to an understanding at the molecular level of the development of a nervous system with diverse neuronal populations that are specifically interconnected to distinct input neurons and target tissues as required for the performance of a complex regulatory function.

Animals↗

PubMed1961

Effect of morphine on some sympathetically innervated effectors.

Morphine, in doses of 0.5 to 55 mg/kg, inhibited contraction of the nictitating membrane of the cat following stimulation of the postganglionic sympathetic nerve fibres. Morphine was more effective at low than at high frequencies of stimulation, independently of the size of contraction of the membrane; the speed of contraction was reduced at all frequencies. Cocaine potentiated the contraction of the nictitating membrane following nerve stimulation more at low than at high frequencies, and antagonized the action of morphine. These findings, and the absence of an effect of morphine on the action of injected noradrenaline, make it likely that morphine interferes with the release of noradrenaline from the postganglionic nerve endings in the nictitating membrane. Morphine had no effect on the cardioaccelerator action of the cardiac nerves and inconsistent results were obtained on the emptying of the spleen after stimulation of the splenic nerves.

Animals↗

PubMed1997

Calbindin D28K-immunoreactivity identifies distinct subpopulations of sympathetic pre- and postganglionic neurons in the rat.

Neurons performing the same function can be identified immunohistochemically because they often share the same neurochemistry. The distribution of calcium-binding proteins, like calbindin, has been used previously to identify functional subpopulations of neurons in many parts of the nervous system. In this study we have investigated the distribution of calbindin D28K-immunoreactivity in subpopulations of sympathetic preganglionic neurons in the intermediolateral nucleus of the rat spinal cord. The majority of calbindin D28K-immunoreactive preganglionic neurons also had co-localised nitric oxide synthase, although a population of preganglionic neurons in the mid- to low thoracic intermediolateral nucleus expressed only calbindin D28K-immunoreactivity. Retrograde-tracing studies showed that calbindin D28K-immunoreactive neurons projected to the superior cervical and stellate ganglia, with smaller numbers of cells projecting to the lumbar sympathetic chain and superior mesenteric ganglia. Very few calbindin D28K-immunoreactive neurons projected to the inferior mesenteric ganglion, and none projected to the adrenal medulla. The distribution of calbindin D28K-immunoreactive terminals and postganglionic neurons in the superior cervical and stellate ganglia was also investigated. Many postganglionic neurons were calbindin D28K-immunoreactive, and most of these lacked neuropeptide Y-immunoreactivity. Calbindin D28K-immunoreactive nerve terminals were common and formed dense pericellular baskets around many postganglionic neurons, including some of those that were calbindin D28K-immunoreactive, but only rarely formed pericellular baskets around neuropeptide Y-immunoreactive neurons. The function of some of the classes of postganglionic neurons that were the target of calbindin D28K-immunoreactive preganglionic terminals was determined by combining immunohistochemistry with retrograde-tracer injections into a range of peripheral tissues. Calbindin D28K-immunoreactive nerve terminals, with co-localised nitric oxide synthase-immunoreactivity, surrounded secretomotor neurons projecting to the submandibular salivary gland and pilomotor neurons projecting to skin, but did not surround neurons projecting to brown fat or vasomotor neurons projecting to the skin, muscle, or salivary glands.

Adipose Tissue, Brown↗

PubMed2003

The peripheral sympathetic nervous system is the major target of cannabinoids in eliciting cardiovascular depression.

Our objective was to identify the sites of interaction of cannabinoids with cardiovascular sympathetic regulation in the rat. Effects on sympathetic tone were first determined in anaesthetised animals following i.v. administration of the drugs. Central effects were evaluated in anaesthetised rats receiving microinjections of cannabinoids into brain stem nuclei. Peripheral effects were identified in pithed rats with electrically stimulated sympathetic outflow. In anaesthetised and artificially ventilated rats, i.v. injection of the cannabinoid agonists WIN55212-2 and CP55940 decreased mean arterial pressure, heart rate and the plasma noradrenaline concentration. These effects were antagonized by the CB(1) cannabinoid receptor antagonist SR141716A. The bradycardia was abolished by the muscarinic acetylcholine receptor antagonist methylatropine. The decreases in mean arterial pressure and heart rate caused by cannabinoids in ventilated rats were much less pronounced than in spontaneously breathing rats. Microinjection of WIN55212-2 into the nucleus tractus solitarii had no effect. Microinjected into the rostral ventrolateral medulla oblongata, WIN55212-2 lowered mean arterial pressure slightly without changing other parameters. In pithed rats, WIN55212-2 inhibited the increases in mean arterial pressure, heart rate and the plasma noradrenaline concentration evoked by electrical stimulation of the sympathetic outflow. Our results show that activation of CB(1) cannabinoid receptors induces sympathoinhibition and enhancement of cardiac vagal tone, leading to hypotension and bradycardia. Presynaptic inhibition of noradrenaline release from terminals of postganglionic sympathetic neurons is the major component of the sympathoinhibition, but an effect in the rostral ventrolateral medulla oblongata may also contribute. The cannabinoid-evoked cardiovascular depression depends strongly on the respiratory state of the animals.

Animals↗

PubMed2001

Differential control of sympathetic outflow.

With advances in experimental techniques, the early views of the sympathetic nervous system as a monolithic effector activated globally in situations requiring a rapid and aggressive response to life-threatening danger have been eclipsed by an organizational model featuring an extensive array of functionally specific output channels that can be simultaneously activated or inhibited in combinations that result in the patterns of autonomic activity supporting behavior and mediating homeostatic reflexes. With this perspective, the defense response is but one of the many activational states of the central autonomic network. This review summarizes evidence for the existence of tissue-specific sympathetic output pathways, which are likely to include distinct populations of premotor neurons whose target specificity could be assessed using the functional fingerprints developed from characterizations of postganglionic efferents to known targets. The differential responses in sympathetic outflows to stimulation of reflex inputs suggest that the circuits regulating the activity of sympathetic premotor neurons must have parallel access to groups of premotor neurons controlling different functions but that these connections vary in their ability to influence different sympathetic outputs. Understanding the structural and physiological substrates antecedent to premotor neurons that mediate the differential control of sympathetic outflows, including those to noncardiovascular targets, represents a challenge to our current technical and analytic approaches.

Adipose Tissue, Brown↗

PubMed2001

Comparison of SSR and QSART in early diabetic neuropathy--the value of length-dependent pattern in QSART.

We evaluated postganglionic sympathetic function using the sympathetic skin response (SSR) and quantitative sudomotor axon reflex test (QSART) on the feet of 31 patients with early diabetic neuropathy and 20 age-matched normal controls. The amplitude of SSR and the sweat volume of QSART were significantly decreased in the diabetic patients. We evaluated the sensitivity of the tests in detecting autonomic failure. Out of 31 patients, 14 (45%) had abnormal SSR (14 absent; 17 present), while 16 of 31 patients (52%) had abnormal QSART (1 absent; 5 absolutely reduced and 10 showed a length-dependent pattern of reduction). More important than differences in sensitivity is the specificity of QSART, which specifically evaluates the postganglionic axon (instead of polysynaptic pathways in SSR) and provides quantitative data on the severity and pattern of autonomic deficit. In normal controls under 65 years of age, there was a significant correlation between the amplitude of SSR and the sweat volume of QSART. However, there was no significant relationship between these in diabetic patients. These results suggest that QSART can evaluate early diabetic neuropathy more precisely than SSR.

Aged↗

PubMed2002

Coherent sympathetic nerve activity in different postganglionic nerves after spinal cord transection in the cat.

In this study, simultaneous discharges were recorded in three nerves originating from different levels of the spinal cord and the correlation between them was analyzed in the absence of the synchronizing input from the brainstem. In acute spinal cats, significant coherence (up to 0.3) was found at low frequencies (<4 Hz) between the vertebral and cardiac nerves and between the vertebral and renal nerves. Coherent discharges were, however, unstable, intermittent, and occurred rarely. In most experiments, it took several hours of observation to capture such an episode. Intrathecal glutamate injections facilitated the occurrence of rhythmic slow waves, which were, however, not correlated. We conclude that spinal sympathetic networks are capable of low frequency synchronization of the activity in different sympathetic outputs.

Animals↗

PubMed1996

Improved neurochemical recovery of 6-hydroxydopamine-lesioned postganglionic sympathetic neurons by nerve growth factor in the adult rat.

Intraplantar injections of nerve growth factor (NGF; five injections of 4 micrograms each in 30 h intervals) were able to locally improve the recovery of the noradrenaline content in 6-hydroxydopamine (6-OHDA)-lesioned sympathetic nerves in adult rats. Whereas 8 days after the 6-OHDA treatment the noradrenaline content in the paw skin was still less than 10% of control, it reached up to 40% of control levels in NGF injected paws. Intraplantar NGF also significantly improved the recovery of the noradrenaline content in the innervating sciatic nerve, but not in distant tissues. The NGF-induced recovery of noradrenergic nerves was independent of the presence of sensory peptidergic afferents and it could not be mimicked by a local inflammatory response known to raise endogenous NGF production. These results show that rather low doses of exogenous NGF were able to locally restore peripheral noradrenergic nerves after an acute neurotoxin lesion.

Age Factors↗