Ganglion-blocking Drugs Research Articles

Augmentation of drug-induced blood pressure increases in rats by amorbarbital.

The effects of amobarbital anaesthesia on blood pressure responses to angiotensin and noradrenaline were determined in rats with chronically implanted venous and aortic catheters. Responses were tested twice on the same day in each rat, first in the conscious state and then during anaesthesia. Blood pressure rises produced by noradrenaline and angiotensin were larger when the rats were anaesthetized with amobarbital than when they were conscious. This enhancement was not characteristic of general anaesthesia since urethane, instead of enhancing, depressed the pressor responses.Blockade of acetylcholine receptors with atropine also increased the response to pressor drugs. However, amobarbital in anaesthetic doses did not affect the response to acetylcholine, indicating that removal of compensatory parasympathetic reflexes was not a major cause of its enhancing effect. The effects of amobarbital on arterial pressure and heart rate were similar to those of the ganglion blocking drug pentolinium. When pressor responses were increased by amobarbital, autonomic ganglia were depressed as indicated by the loss of the response to nicotine. These findings suggest that amobarbital enhances blood pressure responses to noradrenaline and angiotensin by blocking autonomic ganglia.

Measurement of fecal output in rats.

A test was developed to quantify fecal output in rats. Narcotic analgesic (diphenoxylate, morphine), ganglionic blocking (mecamylamine) and anticholinergic drugs (atropine) decreased fecal output. Compounds with direct smooth muscle depressant properties (papaverine, mebeverine) did not alter fecal output. Several other drugs were also evaluated. The rat animal model is useful for assessing the effects of various drugs in altering fecal output.

Some effects of hexamethonium and tetraethylammonium at a neuromuscular junction of the chicken

The effects of the ganglion-blocking drugs hexamethonium and tetraethylammonium were studied on the responses of the chick biventer cervicis muscle to acetylcholine and carbachol, and their anticholinesterase activities were measured using the same muscle as the source of enzyme. Large concentrations of hexamethonium and tetraethylammonium had little effect on responses to acetylcholine but blocked responses to carbachol. However, responses to acetylcholine were blocked by these compounds in the presence of physostigmine. Essentially similar effects were produced in chronically denervated muscles. Large concentrations of hexamethonium and tetraethylammonium possessed anticholinesterase activity in chick muscle. It was concluded that the main action of hexamethonium and tetraethylammonium in the chick biventer cervicis muscle is a post-junctional antagonistic action which, in the presence of acetylcholine, is masked by a weak anticholinesterase activity, and that these drugs owe little of their effects to an action nervous tissue.

Synaptic potentials recorded by the sucrose-gap method from the rabbit superior cervical ganglion.

1. Compound ganglionic potentials evoked by stimulation of the preganglionic nerves to the superior cervical ganglion of the rabbit were recorded by the sucrose-gap method.2. When the distal part of the ganglion was bathed in flowing isotonic sucrose solution or sodium-deficient solutions, ganglionic action potentials were no longer evoked, only large synaptic potentials.3. The compound synaptic potential, which remained unaltered for more than 1 h, originated in a population of cells at the interface between the Krebs and sucrose solutions. Hexamethonium reduced the size but did not alter the time course of the synaptic potential.4. It is suggested that a higher concentration of sodium ions is required for the generation of ganglionic action potentials than for either conduction in the postganglionic axons or production of synaptic potentials.5. When lithium replaced sodium in the solution bathing the distal part of the ganglion, the synaptic potential was greatly reduced in amplitude. Impulse propagation in the postganglionic axons was only slightly impaired when lithium replaced sodium in the solution bathing the axons.6. A quantitative assessment of the potency of the ganglion-blocking drugs nicotine, pentolinium, hexamethonium and pempidine was made by measuring the depression of the synaptic potentials produced by bathing the distal part of the ganglion in flowing isotonic sucrose solution. The concentrations which produced a 50% depression were 8.1 muM nicotine, 26.5 muM pentolinium, 111 muM hexamethonium and 22.2 muM pempidine.

Studies on the thyroid in spontaneously hypertensive rats. II. Effect of some experimental procedures on thyroid activity.

1. Thyroid activity in SHR remained elevated even after the difference in adrenocortical activities between SHR and control rats was eliminated by adrenalectomy with supplements of NaCl and small doses of hydrocortisone. 2. Thyroid activity in SHR remained elevated even after the administration of hexamethonium, a ganglionic blocking drug. 3. Acute cold exposure (6-8°C, 6 hours) stimulated thyroid activity in SHR but not in control rats. This phenomenon was not prevented by adrenalectomy (with NaCl and hydrocortisone supplement) or by hexamethonium administration. 4. Chronic cold exposure (2-10°C, 6-12 weeks) stimulated thyroid activity more in SHR than in control rats. 5. Emotional stress (restraint for one hour a day for two days) depressed thyroid activity in control rats but not in SHR. The response was not affected by adrenalectomy (with NaCl and hydrocortisone supplement). 6. These results (1, 2) indicate that the elevated thyroid activity in SHR is mediated by neither the adrenal cortex nor the autonomic nervous system. 7. The significance of the different effects of cold exposure and restraint on the thyroid activi-ty in SHR (3, 4, 5) is discussed.

Effects of ganglionic and cholinergic blocking drugs on the pressor response to central vagal stimulation.

Effects of ganglionic and cholinergic blocking drugs on the pressor response to central vagal stimulation.

Nerve‐mediated excitation and inhibition of the smooth muscle cells of the avian gizzard

1. The electrical events evoked in smooth muscle cells of the chick and pigeon gizzards by vagal, perivascular sympathetic and transmural stimulation were recorded with intracellular micro-electrodes.2. Single stimulating pulses applied to the extrinsic nerves, or to intrinsic fibres, produced excitatory junction potentials (E.J.P.s) which were blocked by hyoscine. Repetitive stimulation caused facilitation of E.J.P.s and, at higher frequencies, summation. When the tissue was well oxygenated, maximal stimulation evoked action potentials and the tissue contracted. If the tissue was allowed to become anoxic, action potentials were blocked and thus junctional transmission could be observed uncomplicated by tissue contraction.3. Cholinergic E.J.P.s appeared to be due to stimulation of both post-ganglionic neurones and the pre-ganglionic input to post-ganglionic neurones, since ganglion-blocking drugs abolished the late phase of complex E.J.P.s while leaving unaffected their initial components.4. Repetitive perivascular sympathetic stimulation, after cholinergic E.J.P.s had been blocked by hyoscine, evoked a slow, long-lasting depolarization of the muscle cells. This depolarization was blocked by guanethidine (5 x 10(-6) g/ml.) and was mimicked by noradrenaline (10(-7) g/ml.).5. Under non-anoxic conditions, the tissue underwent rhythmical contractions which were associated with action potential firing. When the tissue was anoxic action potentials were not seen, but spontaneous membrane depolarizations resembling E.J.P.s were observed. Spontaneous miniature excitatory junction potentials (M.E.J.P.s) were observed only infrequently whether the tissue was well oxygenated or not.6. Single stimulating pulses applied to extrinsic or intrinsic nerves frequently evoked inhibitory junction potentials (I.J.P.s) in smooth muscle cells of the gizzards of both birds. I.J.P.s were blocked by tetrodotoxin (10(-7) g/ml.). Repetitive stimulation of inhibitory nerves gave rise to a membrane hyperpolarization; when stimulation was stopped the membrane potential showed rebound depolarization.7. These results are discussed in terms of the autonomic innervation of the avian gizzard, and possible explanations of the various types of activity observed are considered.

Modification of nicotine toxicity by pretreatment with different drugs

Sub-lethal doses of nicotine have been shown to protect mice from the lethal effects of subsequently administered doses of the same drug. The evidence suggests that a metabolic product of nicotine is responsible for the protective action. In an attempt to identify this metabolite it was shown that cotinine had no protective action but that nicotine N-oxide and also the reduction product of cotinine both conferred some protection. The pharmacological basis of the protective effect is not clear but it may involve ganglion-blocking activity; the ganglion-blocking drugs hexamethonium and pempidine also protected mice from the lethal effects of nicotine.

The actions of some cholinomimetic drugs on the isolated taenia of the guinea-pig caecum.

1. The actions on the taenia of 4-(m-chlorophenylcarbamoyloxy)-2-butynyl-trimethylammonium chloride (McN-A-343), N-benzyl-3-pyrrolidyl acetate methobromide (AHR-602), tetramethylammonium (TMA) and choline phenyl ether have been examined and compared with the actions of acetylcholine, nicotine and 1,1-dimethyl-4-phenylpiperazinium (DMPP).2. Responses of the taenia to these agonists are quantitatively and often qualitatively dependent on the tone of the preparation. A method is described which makes allowance for the effect of tone on heights of contractions.3. Acetylcholine, McN-A-343 and AHR-602 produced only contractions; TMA produced contractions or biphasic responses; and choline phenyl ether, nicotine and DMPP produced contractions, relaxations or biphasic responses.4. The mode of action of these compounds has been analysed by means of hyoscine, ganglion-blocking drugs, tetrodotoxin and local anaesthetics.5. It is concluded that acetylcholine, McN-A-343, AHR-602, TMA and choline phenyl ether act on muscarinic receptors in the smooth muscle. Choline phenyl ether has an additional action on nicotinic receptors of cholinergic neurones. Nicotine and DMPP act on nicotinic receptors of cholinergic neurones and of inhibitory neurones. An action on the latter is sometimes also seen with TMA and choline phenyl ether.6. With nicotine or DMPP, and TMA or choline phenyl ether in the presence of hyoscine, part of the contraction phase of biphasic responses (in which a contraction follows relaxation) is best explained as being triggered by the initial relaxation-that is, as a "rebound contraction".7. None of the compounds tested appeared to exert an atropine-sensitive action on neurones.8. In the presence of hyoscine high concentrations of agonists can act on sites not involved with lower concentrations.

Evidence for muscarinic receptors in the adrenal medulla of the dog.

1. The release of catecholamines from the adrenal medulla by the cholinergic drugs was monitored by the perfusion pressure rise in autoperfused and sympathetically denervated hindlimbs of the dog.2. Acetylcholine, dimethylphenylpiperazinium (DMPP) and methacholine, given in relatively small doses into the aorta proximal to the blood supply to the adrenal glands, caused a marked rise in perfusion pressure which was due to the release of catecholamines from the adrenal medulla.3. Atropine (1 mg/kg intravenously) blocked the pressor response to methacholine only. The ganglion-blocking agents (mecamylamine 4-5 mg/kg or hexamethonium 10 mg/kg) given subsequently blocked the pressor responses to the other two cholinergic drugs. The ganglion-blocking agents, when given before atropine, blocked the pressor action only of DMPP. These agents partly depressed, rather than potentiated, the pressor response to methacholine.4. The results suggest that muscarinic as well as nicotinic receptors are present in the adrenal medulla of the dog.5. Neither atropine nor ganglion-blocking drugs alone reduced the pressor response to acetylcholine. It is postulated that the blockade of one set of receptors makes more acetylcholine available for the other set of receptors and so inactivation of the former receptors are compensated by the increased release through the activation of the latter's.

An analysis of possible nervous mechanisms involved in the peristaltic reflex.

1. The effects of drugs on peristalsis and on the contractions of the two muscle coats of the isolated guinea-pig ileum in response to co-axial electrical stimulation have been studied.2. Co-axial stimulation (0.1 msec pulses) never produces simultaneous contraction of both muscle coats. When one muscle contracts, the other either relaxes or remains quiescent.3. The circular muscle contraction has two components. The first is reflex in origin and is brought about either by distension of the gut with increasing intraluminal filling or by the contraction of the longitudinal muscle in response to electrical stimulation at low frequency (1/sec), provided this raises the intraluminal pressure to the threshold for eliciting the circular muscle contraction. As the circular muscle contracts, the longitudinal muscle relaxes although stimulation continues. If the circular muscle contraction is prevented by reducing the intraluminal filling, or by adding a ganglion-blocking drug, the longitudinal muscle remains contracted until withdrawal of the stimulus.4. In the presence of hyoscine, the reflex contraction of the circular muscle is unimpaired but, since the longitudinal muscle contraction is abolished, a higher intraluminal pressure is required to elicit the reflex.5. The second component of the circular muscle contraction appears in response to electrical stimulation at high frequency (3-10/sec), upon withdrawal of electrical stimulation. This delay indicates the simultaneous stimulation of a dominant inhibitory innervation.6. The excitatory nerves to the circular muscle require a higher frequency of stimulation than those to the longitudinal muscle, which respond to single shocks.7. Cholinergic blocking agents (hyoscine, morphine, hemicholinium and botulinum toxin) antagonize the responses of the longitudinal muscle to co-axial stimulation without affecting those of the circular muscle, thus suggesting that the excitatory fibres to the circular muscle are not cholinergic. Prostaglandins (E(1) and E(2)) selectively antagonize the circular muscle contractions evoked by co-axial stimulation. Tetrodotoxin blocks both longitudinal and circular muscle responses.8. Dimethylphenylpiperazinium (DMPP) and 5-hydroxytryptamine (5-HT) stimulate ganglia but have no direct action on the smooth muscle of guinea-pig ileum.9. During a maintained contraction of the longitudinal muscle in the presence of high concentrations of acetylcholine (2.5 x 10(-7) to 10(-6) g/ml.) a contraction of the circular muscle accompanied by a relaxation of the longitudinal muscle is elicited by distension of the gut, and by co-axial stimulation. Similar reciprocal responses are produced by 5-HT or by DMPP and they are finally blocked by DMPP.10. These results are consistent with the hypothesis that in the myenteric plexus there exists an arrangement of nerves which ensures that the two muscle coats of the intestine do not contract simultaneously but are activated reciprocally so that when one muscle layer contracts the other relaxes or is prevented from contracting.

Antagonism by antimuscarinic and ganglion-blocking drugs of some of the behavioural effects of nicotine.

The effects of nicotine on bar-pressing behaviour in the rat are blocked by mecamylamine. The depressant phase of the effect is blocked by atropine, supporting the conclusion that this depression is mediated by released acetylcholine. The quaternary compounds chlorisondamine and atropine methylnitrate also antagonise the behavioural effects of nicotine but the doses required for this are far in excess of those which are effective peripherally, suggesting that the sites of interaction are central.

The effect of vagal block or hexamethonium on gastric secretion in the dog.

Because of relevance to the operation of vagotomy in man, and to ‘medical vagotomy’ tests attempting to forecast the results of surgery, we have made a study in the dog of the effects of (1) blocking the vagus nerves with local anaesthetic and (2) injecting intravenously a ganglion-blocking drug. Gastric secretion was stimulated with both high and low doses of histamine and gastrin in dogs equipped with either a Heidenhain or a Pavlov pouch. Although the blocking procedures abolished acid and pepsin secretion caused by a pure vagal stimulant (2-deoxy-D-glucose) they had less effect against gastrin, and still less against histamine. The implications of these results are discussed.

Effect of ganglionic blocking on plasma renin activity in exercising and pain-stressed rats.

AbstractThe effect of ganglionic blocking on piasma renin activity and plasma sodium concentration during exercise and pain stress were studied in rats. 20 female albino rats were exercised by swimming and 16 received intramuscular injections of 1 ml 10% NaCl. Half of the animals in each group were pretreated with a ganglionic blocking drug (Ansolysen®). In both groups there was a significantly lower plasma renin activity in the ganglion‐blocked animals compared with their untreated controls, which indicates the importance of the sympathetic system for renin release. The findings suggest that changes in plasma sodium concentration are of minor importance compared with sympathetic activity.

Gastrointestinal Actions of Metoclopramide

Summary The gastrointestinal actions of metoclopramide [ N -(diethylaminoethyl)-2-methoxy-4-amino-5-chlorobenz amide] have been investigated in experimental animals. This compound was found to stimulate gastric contractile activity in anesthetized and unanesthetized dogs and to accelerate stomach emptying in rats and monkeys. No significant increase in gastric acid secretion could be demonstrated in either rat or dog. The gastric motor stimulation was antagonized by anti cholinergics and morphine, but was not blocked by vagotomy or a ganglionic blocking drug. The action of metoclopramide appears to involve activation of intramural cholinergic neurons respon sible for modifying gastric motility but notacid secretion, either by a direct stimulation or by removal of inhibitory influences.

Inhibitory effect of angiotensin on the intestinal motility of the cat and its relation to sympathetic nervous system.

(4 figures) It is reported by KHAIRALLAH and PAGE (1961) that angiotensin has a direct and indirect action on the isolated guinea-pig ileum. The indirect action of angiotensin is mainly mediated by cholinergic nerves since atropine and ganglion blocking drugs were abIe to block partialIy its contractile action. These results were confirmed by ROBERTSON and RUBIN (1962). Recently a number of papers have been published concerning the interaction of angiotensin with sympathetic nervous system. FELDBERG and LEWIS (1964, 1965) showed that angiotensin is a potent releaser of catecholamines from adrenal medulla. Beside this effect it has been also shown that angiotensin stimulates the superior cervical ganglion of the cat (LEWIS and REIT, 1964,1965, 1966; PANISSET ef al., 1966; TRENDELENBURG, 1966). Some recent investigations about the stimulating effect of angiotensin on the isolated vascuIar smooth muscle preparations suggest that part of its action is mediated through the release of catecholamines from tissues (DISTLER et al., 1965; SCHUMANN and GUTHER, 1967). On the other hand FELDBERG and LEWIS (1965) observed that large doses of angiotensin given intravenously produce a delayed contraction of the denervated nictitating membrane of the adrenalectomized cats. They referred this effect to a possible action of angiotensin on adrenergic nerve endings.

Efeito do hexametônio sobre a motilidade do duodeno de cães pré-tratados pela atropina

The authors studied the behavior of duodenum in atropinized dogs, “in situ”, under the effects of ganglionic blocking drugs. Only Hexamethonium restores the tonus and the motility of the small intestine segment studied. Two explanations were proposed: 1 — Hexamethonium inhibits the “main” ganglionic colinoceptive site and determines that the pre-sinaptic impulses pass through an alternate pathway of transmission, not blocked by Atropine, and restores the colinergic control in the intestinal tract. 2 — The inhibition of the “main” pathway of transmission in sympathetic autonomic ganglia elicits the absence of the sympathetic preponderance and restores the equilibrium broken by the previous administration of Atropine.

Ganglionic blocking properties of epinephrine and related amines

Depression of transmission through the superior cervical ganglion after intra-arterial injection of epinephrine differs from the depression which follows administration of classic ganglionic blocking drugs. Epinephrine (E) caused a greater depression of transmission at low stimulus frequencies than at high stimulus frequencies. The S-1 and S-2 spikes and P potential of the ganglion action potential were relatively sensitive to the effect of E, but the S-4 spike was resistant. Complete block of transmission was not obtained with doses of E up to 1000 μg. No difference in block was observed with maximal or submaximal stimulus strengths. The E effect was antagonized by phenoxybenzamine. Norepinephrine (NE) and dopamine were less potent than E in reducing ganglionic transmission. Tyramine had a biphasic effect. A depression of transmission, qualitatively different from E and resistant to antagonism by phenoxybenzamine, occurred immediately after injection. After a short recovery phase, another depression (2–5 min after injection) occurred. The late depression was qualitatively similar to the E effect. E usually caused a small depolarization of the ganglion, but this depolarization was unrelated to the time course or magnitude of the depression of the S-2 spike.

Effects of ganglionic blocking drugs on blood glucose, amino acids, free fatty acids, free fatty acids and catecholamines at exercise in man.

AbstractCarlsten, A., J. Häggendal, B. Hallgren, R. Jagenburg, A. Svanborg and L. Werkö. Effects of ganglionic blocking drugs on blood glucose, amino acids, free fatty acids and catecholamines at exercise in man. Acta physiol. scand. 1965. 64. 439–447. – The influence of exercise of submaximal load on the arterial concentration of catecholamines, free fatty acids (FFA), and amino acids was studied in 6 young healthy men. The noradrenaline (NA) level increased as a rule successively but the low adrenaline (A) level was unchanged. After 14–18 min of work there was no change in the total FFA level, but among the individual FFA the percentage of stearic and oleic acid decreased, whereas that of palmitic, palmitoleic and linoleic acid increased. The total amino nitrogen level increased and among the individual amino acids there was a marked elevation in alanine. When the exercise was performed during the infusion of ganglionic blocking drugs the increase in NA was abolished or less marked but the changes in the arterial concentrations of glucose, lactic acid, pyruvic acid, amino acids and FFA were similar as without drugs. These results indicate that the role of the sympathetic nervous system is of minor importance for the regulation of the free fatty acid level in serum during exercise.

INDEPENDENT CHOLINERGIC AND ADRENERGIC MECHANISMS IN THE GUINEA‐PIG ISOLATED NERVE VAS DEFERENS PREPARATION

British Journal of Pharmacology and ChemotherapyVolume 24, Issue 3 p. 641-650 Free Access INDEPENDENT CHOLINERGIC AND ADRENERGIC MECHANISMS IN THE GUINEA-PIG ISOLATED NERVE VAS DEFERENS PREPARATION K. P. BHARGAVA, K. P. BHARGAVA Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this authorK. KAR, K. KAR Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this authorSURENDRA S. PARMAR, SURENDRA S. PARMAR Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this author K. P. BHARGAVA, K. P. BHARGAVA Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this authorK. KAR, K. KAR Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this authorSURENDRA S. PARMAR, SURENDRA S. PARMAR Upgraded Department of Pharmacology and Therapeutics, K.G. Medical College, Lucknow University, IndiaSearch for more papers by this author First published: June 1965 https://doi.org/10.1111/j.1476-5381.1965.tb01620.xCitations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat REFERENCES Axelrod, J. (1959). Metabolism of epinephrine and other sympathomimetic amines. Physiol. Rev., 39, 751– 776. Bentley, G. A. 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