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PubMed1996

Reduced capacity of cardiac efferent sympathetic neurons to release noradrenaline and modify cardiac function in tachycardia-induced canine heart failure.

To investigate the capacity of efferent sympathetic neurons to modulate the failing heart, stellate ganglion stimulation was performed in dogs with biventricular heart failure induced by rapid ventricular pacing (240 beats/min) for 4-6 weeks. Less noradrenaline was released from cardiac myoneural junctions into coronary sinus blood in response to left stellate ganglion stimulation in anesthetized failing heart preparations (582 pg/mL, lower and upper 95% confidence intervals of 288 and 1174 pg/mL, n = 19) compared with healthy heart preparations (6391 pg/mL, 95% confidence intervals of 4180 and 9770 pg/mL, n = 14; p < 0.001). There was substantial adrenaline extraction by failing hearts (49 +/- 6%), although it was slightly lower than in healthy heart preparations (65 +/- 9%, p = 0.055). In contrast with healthy heart preparations, no net release of adrenaline occurred during stellate ganglion stimulation in any of the failing heart preparations, and ventricular tissue levels of adrenaline fell below the sensitivity limit of the HPLC technique. In failing heart preparations, maximal electrical stimulation of right or left stellate ganglia resulted in minimal augmentation of left ventricular intramyocardial (17%) and chamber (12%) systolic pressures. These indices were augmented by 145 and 97%, respectively, following exogenous noradrenaline administration. Thus, the cardiac efferent sympathetic neurons' reduced capacity to release noradrenaline and modify cardiac function can contribute to reduction of sympathetic support to the failing heart.

Animals↗
PubMed1999

ATP as a source of interstitial adenosine in the rat heart.

The contribution of neuronal ATP to interstitial adenosine levels was investigated in isolated perfused rat hearts. Ventricular surface transudates, representing interstitial fluid, were analyzed for norepinephrine, ATP, and adenosine. Exocytotic release of norepinephrine was induced by electrical stimulation of cardiac efferents emanating from the stellate ganglion. Ganglion stimulation increased contractility, interstitial norepinephrine, ATP, and adenosine. Interstitial adenosine was 11- to 27-fold higher than interstitial ATP, suggesting that the released ATP is unlikely the only source of adenosine. In the presence of AOPCP (alpha,beta-methyleneadenosine 5'-diphosphate), an ecto-5'-nucleotidase inhibitor, the ganglion-stimulated increase in interstitial ATP and adenosine reached levels similar to those in the absence of AOPCP, also suggesting that adenosine does not derive from extracellular ATP. The perfusate Ca2+ was raised from 1 to 4 mM to determine the importance of the enhanced contractile function on the levels of norepinephrine, ATP, and adenosine. The results were increases in contractility and interstitial norepinephrine, ATP, and adenosine, which were not suppressed with atenolol, indicating a norepinephrine-independent release of ATP and adenosine. Reserpine treatment and administration of guanethidine depleted the catecholamine stores and diminished the catecholamine release, respectively. However, neither agent altered Ca2+-induced increases in ATP and adenosine. It is concluded that the amount of neuronal-derived ATP is low and most likely does not contribute significantly to interstitial levels of adenosine. Furthermore, elevations in interstitial norepinephrine, ATP, and adenosine are associated with neuronal-independent increases in contractile function.

Adenosine↗
PubMed1989

Beta 2-adrenoceptor stimulation inhibits ganglionic transmission in ferret trachea.

To study the effect of beta-adrenoceptor stimulation on the transmission through airway parasympathetic ganglia, we used an in vitro nerve-muscle preparation of ferret trachea. Isometric muscle contractions were induced for 20 s every 2 min alternating with postganglionic activation by electrical field stimulation (EFS) or with preganglionic activation by direct nerve stimulation (DNS). The pulse frequency was always 12 Hz. A possible modulation of ganglionic transmission was assessed by comparing contractions induced by DNS to contractions induced by EFS. In 9 experiments isoprenaline initially reduced the response to EFS and DNS to the same extent, indicating an effect on postganglionic structures. After 20-30 min exposure the response to preganglionic activation by DNS was further reduced indicating an inhibition of ganglionic transmission. The concentration/response relationship for the ganglionic effect of isoprenaline was shifted about ten times to the right by 0.1 microM propranolol (n = 5) and by a beta 2-adrenoceptor-antagonist (0.1 microM ICI 118.551) (n = 8), whereas a beta 1-adrenoceptor-antagonist (10 microM practolol) had no, or only slight, effect. In two experiments pretreatment by 0.1 microM phenoxybenzamine for 20 min did not prevent ganglionic inhibition by 0.3 microM isoprenaline. We conclude that parasympathetic ganglia in ferret trachea have beta-adrenoceptors mediating inhibition of ganglionic transmission, and that these probably are of the beta 2 type. Tentatively these receptors could be operated upon by circulating catecholamines.

Adrenergic beta-Agonists↗
PubMed1988

Systolic pressure gradients between the wall of the left ventricle, the left ventricular chamber, and the aorta during positive inotropic states: implications for left ventricular efficiency.

To study systolic pressure gradients developed between the left ventricular wall, its chamber, and the aortic root, in one group of dogs left ventricle ventral wall intramyocardial pressure, left ventricular outflow tract pressure, and aorta pressure were compared with aortic flow as well as left ventricular dimension changes during control conditions as well as during positive intropic states induced by isoproterenol, stellate ganglion stimulation, and noradrenaline. In another group of dogs systolic pressures in the ventral wall of the left ventricle, the main portion of the left ventricular chamber, and the aorta were compared with aortic flow during similar interventions, before and after the administration of phentolamine. Pressure gradients between the wall of the left ventricle and the outflow tract of the left ventricle were minimal during control states, but during the three positive inotropic states were increased significantly. In contrast, pressure gradients between the outflow tract of the left ventricle and the aortic root were insignificant during positive inotropic states; those between the wall and main portion of the chamber were only significantly different during left stellate ganglion stimulation. The data derived from these experiments indicate that useful peak power output of the left ventricle (systolic aortic pressure X flow) is unchanged following isoproterenol infusion, but is increased by stellate ganglion stimulation and noradrenaline. The useful peak power output index (an index of left ventricular efficiency derived by dividing useful peak power output by peak intramyocardial pressure) was reduced more by isoproterenol than the other two interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Vasodilatation of arterioles by acetylcholine released from single neurones in the guinea-pig submucosal plexus.

The nervous control of arterioles in the guinea-pig submucosal plexus was studied. Outside diameters of arterioles were recorded using a video-monitoring system. Changes in arteriolar diameter in response to electrical stimulation of single neurones or ganglia in the plexus were measured. 2. When the arteriole was pre-constricted with the prostaglandin analogue U46619 or with phenylephrine, electrical stimulation (2-20 Hz, 10 s) of a ganglion dilated the blood vessel. This vasodilatation was abolished by tetrodotoxin or by cutting the fine nerve strands running between the ganglion and the arteriole. 3. The vasodilatations caused by ganglionic stimulation were blocked by the muscarinic antagonists atropine, pirenzepine, (11[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H- pyrido[2,3-b][1,4]benzodiazepine-6-)-one (AFDX-116), 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP) and hexahydrosilodifenidol (HSDF). IC50 values for the inhibition of nerve-evoked vasodilatation by pirenzepine, AFDX-116 and HSDF were 500 nM, 4 microM and 25 nM respectively. Physostigmine (1 microM) increased the dilatation by 90%. 4. Muscarine dilated all submucosal arterioles; the concentration causing half-maximum effects was 200 nM. Muscarinic vasodilatations were inhibited by pirenzepine, AFDX-116, and HSDF in a competitive manner; dissociation equilibrium constants determined by Schild analyses were 125 nM, 1.3 microM and 4 nM respectively. 5. Gossypol, an irreversible inhibitor of the production of endothelium-derived relaxing factor (EDRF), did not reduce the vasodilatation produced by either ganglionic stimulation or muscarine in submucosal arterioles. 6. Intracellular recordings were made from submucosal neurones and action potentials were elicited by depolarizing current pulses (10 ms duration, 10 Hz/10 s). In seven neurones vasodilatation was associated with intracellularly evoked action potentials; this vasodilatation was blocked by pirenzepine. Cell bodies of reidentified vasodilator neurones were subsequently shown to contain immunoreactive choline acetyltransferase. 7. These results show that cholinergic neurones in the submucosal plexus project to submucosal arterioles and that they release acetylcholine onto muscarinic receptors to produce vasodilatation. The muscarinic receptor activated by nerve-released acetylcholine is the M3 subtype and its location appears to be on the vascular smooth muscle rather than the endothelium.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1962

An eserine-like action of chloral hydrate.

The intra-arterial injection of chloral hydrate potentiated the transmission of nerve impulses through the cat superior cervical ganglion, antagonized the ganglionblocking action of hexamethonium, and greatly enhanced the ganglion-stimulant action of acetylcholine. Effects on the ganglion-stimulant actions of carbachol, nicotine, tetramethylammonium and potassium chloride were slight or absent. Chloral hydrate itself usually had no direct stimulant action. The neuromuscular-blocking action of tubocurarine on the isolated rat diaphragm preparation was completely and rapidly reversed by chloral hydrate. This reversal was prevented by previoustreatment of the muscle with neostigmine. Chloral hydrate potentiated the actions of acetylcholine and nicotine on the isolated rabbit duodenum, and, in concentrations exceeding 1 mg/ml., produced a spasm which was abolished by hyoscine but not by mepyramine. It was concluded that these eserine-like effects were manifestations of an anticholinesterase action of chloral hydrate. Neither chloralose nor trichlorethanol showed evidence of this property.

Acetylcholine↗
PubMed1996

Pharmacological analysis of nerves supplying the oesophagus.

Morphological studies indicate that cholinergic, peptidergic and "nitrergic" (nitric oxide releasing) nerves supply the oesophageal muscle. In the present in vitro study, intramural nerves of guinea pig and human oesophagus were activated by means of the ganglion stimulating drug nicotine and electrical field stimulation (EFS) in organ bath experiments. In general, stimulation-induced primary contractions were diminished by atropine, while non-adrenergic, non-cholinergic (NANC) relaxations and after-contractions were inhibited by the NO-synthase inhibitor NG-nitro-L-arginine (L-NNA). Thus we obtained pharmacological evidence for cholinergic muscarinic, as well as nitric oxide mediated mechanisms in the functional innervation of the oesophageal muscle.

Animals↗
PubMed1984

Potentiation by SKF 525A of the pressor responses to catecholamines, oxytocin and carotid occlusion in rats.

The effect of SKF 525A (20 mg/kg i.v.) on pressor responses of various origin was studied. SKF 525A abolished or markedly reduced the pressor responses to ganglionic stimulants (DMPP and McN-A-343), but potentiated those to noradrenaline (in normal and pithed animals), adrenaline, tyramine, oxytocin and carotid occlusion. After recovery of the pressor effect of McN-A-343 from the SKF 525A-induced suppression, the pressor effect of noradrenaline was still further enhanced. The abolition of the pressor responses to ganglionic stimulants is due to the ganglion and adrenal-medullary blocking action of SKF 525A. This action of SKF 525A is of secondary importance for its potentiating effect. It is tentatively suggested that for the SKF 525A-induced potentiation a partial depolarization of arterial smooth muscle membrane resulting from a prolonged release of subthreshold concentrations of catecholamines from tissue stores, may be of primary importance.

Animals↗
PubMed1985

Mucosal responses evoked by stimulation of ganglion cell somas in the submucosal plexus of the guinea-pig ileum.

The effects of electrical field stimulation and tetrodotoxin on the mucosal secretory response were compared in guinea-pig ileal mucosa with and without the submucosal plexus. Short-circuit currents and transmural electrical potential differences were similar in ganglionated and aganglionated tissues. Total tissue conductance was greater after removal of the submucosal ganglia. Electrical field stimulation evoked a tetrodotoxin-sensitive increase in short-circuit current in ganglionated tissues, and little or no response in aganglionated tissues. Both ganglionated and aganglionated tissues responded similarly to carbachol, vasoactive intestinal polypeptide, scorpion venom and alanine. These results suggest that electrical field stimulation of guinea-pig ileum evokes an increase in short-circuit current that reflects chloride secretion by exciting ganglion cell bodies whose axons project to the transporting cells and/or endocrine cells. Direct electrical activation of enteroendocrine cells is not a factor in the stimulus-evoked secretory response.

Action Potentials↗
PubMed1990

[Manifestations of the mobility of sensory neurons of the spinal ganglion after stimulation of its peripheral receptors].

The body of sensory neurons in the frog spinal ganglion++ possesses an active mobility. This is demonstrated as pulsation and changes in its form. The mobility is closely connected with electrogenesis of cells. When an irritation is applied (press of a needle, or application of acetylcholine on the urinary bladder receptors), the neurons of the node respond with an increasing rate of impulse activity. Simultaneously, the mobility of these neurons increases. The character and form of their mobility in response to mechano- and chemoirritation differ from each other. Possible mechanisms of connection between the form of the cell body mobility and the character (active or passive) of its electrogenesis are considered. The mobility of the neurons, together with other morphological signs (tinctorial peculiarities and some others) can serve as an indication of their functional state without application of electrodes in morphological experiments.

Acetylcholine↗
PubMed2002

Assessment of diaphragm function after stellate ganglion block using magnetic stimulation.

Stellate ganglion block is a procedure frequently used for the management of patients with chronic sympathetically mediated pain affecting the arm, neck or head. We studied the effect of stellate ganglion block on ipsilateral phrenic nerve function, and hence diaphragmatic strength, in 11 adult patients with chronic sympathetically mediated pain. Pre- and post-block forced vital capacity (FVC) measurements were recorded using a pneumotachograph and a Magstim nerve stimulator was used to generate pre- and post-block twitch mouth pressures (P(TWM)). This device can be used to stimulate the phrenic nerves and hence the diaphragm. The resulting change in airway pressure was measured at the mouth and has previously been shown to reflect diaphragm strength. There was no statistically significant difference in FVC or P(TWM) pre- or post stellate ganglion block. In conclusion, a stellate ganglion block has no adverse effect on ipsilateral phrenic nerve function or diaphragm strength in healthy adult patients.

Adult↗
PubMed1974

The specificity of some agonists and antagonists for nicotine-sensitive receptors in ganglia.

1 The guinea-pig isolated ileum has been used to estimate the ability of substituted phenylalkylonium salts (related to nicotine) to stimulate or block receptors in ganglia. The effects of hexamethonium were used to indicate which were the most specific ganglion stimulants; these were tested on the blood-pressure of pithed rats and for neuromuscular blocking activity on the rat diaphragm preparation.2m-Hydroxyphenylpropyltrimethylammonium and 3,4-dihydroxyphenethyltrimethylammonium (coryneine, ;quaternary dopamine') were the most active and specific ganglion stimulants but their usefulness in vivo may be limited by their neuromuscular blocking activity. The analogous tertiary compounds are being investigated.3 The affinities of substances which were blocking agents at ganglionic receptors were measured on the isolated ileum with m-hydroxyphenylpropyltrimethylammonium as agonist. The affinities of selected compounds for postganglionic receptors were measured in experiments on the ileum in the presence of hexamethonium and with carbachol as agonist. Some of the compounds were tested for neuromuscular blocking activity on the rat diaphragm.4 Phenylbutyldiethylamine had ganglion-blocking activity greater than pempidine and little postganglionic blocking or neuromuscular blocking activity. Its triethylammonium analogue had higher ganglion-blocking activity but had appreciable neuromuscular blocking activity.5 The aromatic ring system is not essential either for activity or affinity and the effects of substituents are not related to their effects on electron distribution. Stimulant activity is enhanced only by hydroxyl or amino groups in suitable positions; it is not improved by the presence of rigid features (double or triple bonds or a cyclopropane ring) in the side chain. Affinity is slightly increased by chloro or bromo groups in suitable positions but the unsubstituted compounds are among those with the highest affinity. Substituents have similar effects on affinity for postganglionic receptors, though for these receptors the compounds mostly have only about one-tenth of their affinity for ganglionic receptors.

Animals↗
PubMed1997

Role of different subtypes of adrenoceptors in pressor responses to catecholamines released from sympathetic nerve endings.

The role of alpha 1- and alpha 2-adrenoceptors in the vascular effects of catecholamines, either released locally from sympathetic nerve endings (e.g., in vascular smooth muscle) or derived from the adrenal medulla or administered intravenously, was studied using selective antagonists of these adrenoceptors. The ganglionic stimulant dimethylphenyl-piperazinium-iodide (DMPP) exerted dual actions on blood pressure: a rapid and short-term pressor reaction (phase I) resulting from catecholamine release elicited by ganglion stimulation, followed by a more sustained blood pressure elevation (phase II) resulting from the circulating catecholamines released from the adrenal medulla. The selective alpha 2-adrenoceptor, but a not subtype selective, antagonist 7,8-(methylenedioxi)-14-alpha-alloberbane HCl (CH-38083) (50-100 micrograms/kg, IV) significantly (p < 0.05) inhibited the pressor effects of epinephrine and norepinephrine given intravenously and phase II of the DMPP-induced pressor reaction. Idazoxan exerted similar effects, but at higher doses (400-600 micrograms/kg, IV). WB-4101 (50-100 micrograms/kg, IV) and BRL-44408 (2-3 mg/kg, IV), two selective alpha 2A-adrenoceptor antagonists, had the same activity as CH-38083, except did not inhibit the pressor effect of intravenously administered norepinephrine. The alpha 2B-adrenoceptor selective antagonist, ARC-239 (150 micrograms/kg, IV) did not influence phase II of DMPP-induced pressor reaction. Prazosin (200 micrograms/kg, IV), an antagonist of alpha 1 and alpha 2B-adrenoceptors, reduced blood pressure, the pressor response to intravenously administered epinephrine, and phase I of the DMPP-induced pressor effect. In addition, it completely inhibited the pressor responses to DMPP remaining after administration of CH-38083. These results suggest that the postsynaptically located alpha 1- and alpha 2(A and B)-adrenoceptors are involved in pressor response to norepinephrine and epinephrine, and are sensitive and accessible to catecholamines released locally from the axon terminals, and from the circulation to a different extent. These results may have great therapeutical importance in hypertension, for which the involvement of both a high level of circulating and locally released catecholamines may be indicative of the usefullness of a combination (alpha 1- and alpha 2-adrenoceptors- and Ca-channel-blocking agents) therapy.

Adrenergic alpha-Antagonists↗
PubMed1964

OBSERVATIONS ON THE MODE OF ACTION OF SOME CENTRAL DEPRESSANT DRUGS ON TRANSMISSION THROUGH THE CAT SUPERIOR CERVICAL GANGLION.

Methylpentynol, paraldehyde, amylobarbitone and procainamide blocked transmission through the cat superior cervical ganglion, and antagonized the ganglion-stimulating actions of acetylcholine and carbachol injected intra-arterially to the ganglion. Comparison with the effects of tetraethylammonium indicated that the impaired response to acetylcholine could not wholly account for the failure of transmission, which suggested that an impaired release of transmitter substance was a contributory factor. Methylpentynol, paraldehyde and procainamide also blocked the ganglion-stimulating action of potassium chloride. In contrast, amylobarbitone and pentobarbitone did not block the stimulating action of potassium chloride, but antagonized specifically the actions of acetylcholine and carbachol. The anti-acetylcholine activities of the two barbiturate drugs at this site accord with their relative ganglion-blocking activities. It is concluded that the ganglion-blocking action of methylpentynol, paraldehyde and procainamide arises from a nonspecific depression of both presynaptic and postsynaptic elements in the ganglion, but that barbiturate compounds act more specifically on the acetylcholine receptor.

Acetylcholine↗
PubMed1987

The effect of leucine-enkephalin on the peristaltic reflex of the isolated guinea-pig ileum.

Leucine (leu)-enkephalin depresses or inhibits the peristaltic reflex of the isolated guinea-pig ileum. Opiate antagonists (naloxone and nalorphine), choline esters (acetylcholine, methacholine and carbachol), cholinomimetics (muscarine and arecoline) and polypeptides which stimulate peristalsis (eledoisin and angiotensin) antagonize the peristaltic block caused by leu-enkephalin. On the other hand, nicotinic ganglionic stimulants (nicotine and dimethylphenylpiperazine) as well as muscarinic ganglionic stimulants (McN-A-343 and AHR-602) do not restore the peristaltic reflex abolished by leu-enkephalin. Thus the inhibitory effect of leu-enkephalin is due mainly to an action on myenteric ganglia as well as on axon terminals of the myenteric plexus subserving the peristaltic reflex. The inhibitory action of leu-enkephalin may be ascribed to the opiate as well as to the cholinoceptive sites in the nervous elements in the myenteric plexus. The blocking action of leu-enkephalin is not associated with ganglionic muscarinic M-1 receptors as well as with ganglionic nicotinic receptors in the myenteric plexus of the guinea-pig isolated ileum.

Animals↗
PubMed2007

Gradients of atrial refractoriness and inducibility of atrial fibrillation due to stimulation of ganglionated plexi.

INTRODUCTION: The mechanism(s) whereby atrial ectopy induces atrial fibrillation (AF) is still poorly understood. METHODS AND RESULTS: In 12 dogs, we determined the refractory period (RP) along the right atrium (RA) and right superior pulmonary vein (RSPV), and AF inducibility with and without concurrent stimulation of the anterior right ganglionated plexi (ARGP) at the base of the RSPV. Multielectrode catheters were attached to the RSPV and RA with the distal electrodes close to ARGP. The RP and window of vulnerability (WOV), i.e., the longest S1-S2 minus the shortest S1-S2 at which AF was induced, were measured before and during incremental levels of ARGP stimulation. Mapping of the onset of AF was performed using the EnSite mapping system (St. Jude Medical, St. Paul, MN, USA) positioned in the RA. A single premature depolarization (PD) from the RSPV that did not induce AF without ARGP stimulation could do so with ARGP stimulation. The onset of AF consistently arose at the myocardium subtending the ARGP. With GP stimulation, the average WOV at the RSPV-atrial junction was significantly wider than at the RA appendage (65 +/- 27 vs. 8 +/- 17 msec, P < 0.05) or further along the RSPV sleeve (48 +/- 39 vs. 10 +/- 20 msec, P < 0.05). Even without GP stimulation, high intensity (10-20 mA) premature stimuli delivered at the RA appendage induced AF, originating from atrial tissue subtending the ARGP, presumably due to axonal conduction that activated the ARGP. CONCLUSION: GP stimulation, subthreshold for atrial excitation, converts isolated PDs into AF-inducing PDs, suggesting that autonomic tone may play a critical role in the initiation of paroxysmal AF.

Animals↗
PubMed2003

Neuronal control of heart rate in isolated mouse atria.

A novel mouse isolated atrial preparation with intact postganglionic autonomic innervation was used to investigate the neuronal control of heart rate. To establish whether autonomic activation was likely to alter heart rate by modulating the hyperpolarization-activated current (If), the L-type Ca2+ current (ICa,L), or the ACh-activated K+ current (IK,ACh), the effects of nerve stimulation (right stellate ganglion or right vagus, 1-30 Hz) and autonomic agonists (0.1 microM norepinephrine or 0.3 microM carbachol) on heart rate were investigated in the presence of inhibitors of these currents, cesium chloride (Cs+, 1 mM), nifedipine (200 nM), and barium chloride (Ba2+, 0.1 mM), respectively. The positive chronotropic response to stellate ganglion stimulation was reduced by approximately 20% with Cs+ and nifedipine (P < 0.05), whereas the heart rate response to norepinephrine was only reduced with Cs+ (P < 0.05). Ba2+ attenuated the decrease in heart rate with vagal stimulation and carbachol by approximately 60% (P < 0.05). These results are consistent with the idea that sympathetic nerve stimulation modulates If to increase heart rate in the mouse. Activation of ICa,L also appears to contribute to the sympathetic heart rate response. However, the decrease in heart rate with vagal stimulation or carbachol is likely to result primarily from the activation of IK,ACh.

Animals↗