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PubMed1983

Effects of pirenzepine and atropine on vagal and cholinergic gastric secretion and gastrin release and on heart rate in the dog.

To characterize and quantitate pathways of stimulation of gastric secretion via vagal excitation induced by 2-deoxy-D-glucose, we used graded doses of the two muscarinic antagonists, atropine and pirenzepine. Studies were performed in four conscious gastric fistula dogs with antral vagotomy to eliminate the gastrin release component of the vagal response. To further localize the site of action of the antagonists, both were tested against bethanechol, which stimulates secretion at postganglionic sites. Acid and pepsin secretion stimulated by either bethanechol or the vagus were inhibited in a dose-responsive manner by both atropine and pirenzepine, which displayed similar potencies. These data indicate that: 1) the vagus acts on the gastric fundus solely via muscarinic receptors; 2) the muscarinic receptors controlling gastric secretion are of the high-affinity (M-1) subtype; and 3) the vagus is very sensitive to atropine with D50 less than 1.4 nmol/kg. Heart rate was increased up to 120 beats/min above the resting rate by atropine; half-maximal increase was calculated to occur at 10 nmol/kg (ED50). Pirenzepine had a much less potent effect on the heart; the ED50 was 200 to 300 times greater than that for atropine. These data indicate that heart rate is affected by a mechanism acting via a muscarinic receptor pathway that has a low affinity for pirenzepine (M-2 receptor subtype).

Animals↗
PubMed1983

Anticholinergic potency of diphenhydramine (Benadryl) measured against bethanechol in the gastric fistula dog.

We quantitated the gastric secretory anticholinergic effect of diphenhydramine (Benadryl) against graded doses of bethanechol, a cholinergic agonist, which was used to stimulate acid and pepsin secretion. Anticholinergic potency of diphenyhydramine was 10,000 times less than that reported for atropine and was 1,000 times less than the reported potency of diphenhydramine antagonism of histamine H-1 effects.

Animals↗
PubMed1983

Modification of pancreatic carcinogenesis in the hamster model. 7. Inhibitory effect of bethanechol chloride.

Experiments were designed to investigate in the hamster model the effect on pancreatic carcinogenesis of bethanechol chloride (BC), which is known to increase pancreatic protein synthesis in rats. Hamsters received a single (15 mg/kg body weight) dose of BC either before, simultaneously with, or after a single dose of N-nitrosobis(2-oxopropyl)amine (BOP; 20 mg/kg body weight). A second group was treated daily with BC (7.5 mg/kg body weight) for 24 weeks, following BOP. The control groups consisted of animals treated with BOP only, with BC only, and with solvent only. The surviving hamsters were killed 46 weeks after BOP treatment. BC, whether given before, simultaneously with, or after BOP, significantly reduced the incidence of pancreatic ductal/ductular carcinomas. The multiplicity, size, and latency of carcinomas were also affected by BC. A more pronounced inhibition of cancer induction occurred in the group treated daily with BC after BOP. The possible mechanisms involved in the inhibitory action of BC on pancreatic carcinogenesis are discussed.

Animals↗
PubMed1983

Regulation of cyclic GMP levels in nerve tissue.

In rat superior cervical ganglia the regulation of cyclic GMP (cGMP) formation does not involve muscarinic or adrenergic transmitters or receptors. Marked increases in cGMP content during preganglionic axonal stimulation by electric currents, elevated K+, or drugs that cause transmitter release are unaffected by muscarinic and adrenergic receptor blockade. However, the cGMP response does require Ca2+ and intact preganglionic axonal terminals. Two possibilities exist: either cGMP accumulates in the preganglionic nerves or a noncholinergic, nonadrenergic transmitter activates guanylate cyclase in postsynaptic structures. Sodium azide and nitroprusside cause cGMP accumulation in denervated ganglia, which indicates that postsynaptic structures are capable of forming cGMP. In pineal glands elevated [K+]o releases [3H]norepinephrine and causes cGMP accumulation, which suggests a relationship between the two responses and the possibility that cGMP accumulation is involved in autoinhibition of transmitter release. The finding that phentolamine, alpha-adrenergic receptor antagonists, prevent the cGMP response to K+ is compatible with this review. However, clonidine, an alpha-receptor agonist, depresses norepinephrine release but has no effect on pineal gland cGMP. Conversely, large increases in pineal gland cGMP produced by nitroprusside do not affect K+-evoked norepinephrine release. For these reasons it is not possible to relate cGMP to the auto-inhibition of [3H]norepinephrine release that is mediated by prejunctional alpha-adrenergic receptors.

Animals↗
PubMed1983

[The bethanechol test in the diagnosis of neurogenic bladder. 60 cases].

Bethanechol denervation hypersensitivity test seems useful although sometimes disregarded, for the diagnosis of lower neurogenic bladder. Our own experience of 60 patients is presented. When the indications are good (large capacity, hypotonic bladder, clinical suspicion of lower neuron lesion) and when the interpretation is based on a right understanding of its mechanism, this test appears to be very reliable. Except in 4 cases, the difference of pressure is greater than 20 or less than 10 cm H20. Factors susceptible to interfere with its accuracy are summarized. We must admit some discrepancies between the results of this test (exploring the pelvic nerve) and the perineal EMG (exploring the pudendal nerve); this fact is illustrated here. The importance of a wide bladder neck as a radiologic sign of neurogenic bladder is also stressed.

Bethanechol↗
PubMed1983

Prevention of experimental duodenal ulcer in the rat by sucralfate.

We examined the ability of sucralfate to prevent secretagogue induced duodenal ulcer in the rat. Sucralfate was administered orally in dosage schedules of 50 mg, 100 mg or 200 mg before and at 3 and 6 hr after commencing a 24 hr continuous infusion of pentagastrin and bethanechol. The animals were sacrificed at 24 hr and the number and severity of ulcers was scored. Ulcers developed in all 9 control rats, in 8 of 9 on the 50 mg dose, in 4 of 9 on the 100 mg dose, and in only 1 of 9 on the 200 mg dose of sucralfate. We conclude that sucralfate prevents the formation of secretagogue induced duodenal ulcer in the rat.

Aluminum↗
PubMed1983

N,N-dimethyl-10-(3-quinuclidinyl)-2-phenothiazine sulfonamide (LM 24056): mode of action of its gastric antisecretory effect.

The inhibitory effect on gastric secretion of a phenothiazine molecule, N,N-dimethyl-10-(3-quinuclidinyl)-2-phenothiazine sulfonamide (LM 24056), was studied in dogs equipped with gastric fistula (GF) and Heidenhain denervated pouch (HP). LM 24056 was infused intravenously before exogenous stimulations started: the gastric stimulation ws obtained either by gastrin, by combination of gastrin + bethanechol (subthreshold dose) or by histamine. 1. On gastrin-stimulated secretion, preliminary infusion of LM 24056 results in a weak and non-significant reduction on GF acid secretion, while on HP, the inhibition is significant with 1 and 2 micrograms x kg-1 x h-1 of gastrin. The LM 24056 concentrations which produced 50% inhibition (IC50) of acid secretion is close to 0.5 mg x min-1. 2. LM 24056 exerts a strong inhibitory effect on combination gastrin + bethanechol-stimulated acid and pepsin secretions on GH and HP. IC50 is close to 0.25 mg x min-1. 3. LM 24056 is able to delay the histamine-stimulated acid secretion. There are some differences in the gastric inhibitory effects in relation to the moment of LM 24056 administration regarding exogenous stimulant: LM 24056 seems to be able to compete gastrin and to delay the normal histamine stimulation. The most important inhibitory effect is exerted on combination gastrin + bethanechol. LM 24056 could act as an antigastrinic substance.

Animals↗
PubMed1984

alpha- 1 and alpha-2 type adrenoceptors involved in the inhibitory effect of splanchnic nerves on parasympathetically stimulated gastric acid secretion in rats.

The inhibitory effects of the splanchnic nerve on the parasympathetically stimulated gastric acid secretion were analyzed using two different types of alpha adrenergic blocking agents (prazosin and yohimbine). When the gastric acid secretion was increased by infusion of bethanechol, a muscarinic parasympathetic stimulant, the inhibitory effect of stimulation of the splanchnic postganglionic (SP) nerve on the gastric acid secretion was abolished by prazosin, but not by yohimbine. On the other hand, when the gastric acid secretion was increased by stimulation of the vagus nerve, the inhibitory effect of stimulation of the SP nerve on the gastric acid secretion was not abolished by prazosin, but was markedly attenuated by yohimbine. Infusion of clonidine had no effect on the bethanechol-induced gastric acid secretion but did inhibit the vagally stimulated gastric acid secretion in a dose-dependent manner. This effect of clonidine on the vagally stimulated gastric acid secretion was selectively abolished by yohimbine. These results suggest that the SP nerve inhibits the bethanechol-induced gastric acid secretion through alpha-1 type adrenoceptors and inhibits the vagally stimulated gastric acid secretion through alpha-2 type adrenoceptors. We propose that alpha-1 type adrenoceptors are located on the structures peripheral to the parasympathetic nerve terminals, whereas alpha-2 type adrenoceptors are located on the vagally stimulated pathways in the gastric wall. The vagally stimulated pathways display paradoxical resistance to the alpha-1 antagonist, prazosin.

Animals↗
PubMed1984

Study of electromechanical activity of the stomach in humans and in dogs with particular attention to tachygastria.

The relationship between electric and mechanical activities of the gastric antrum was investigated in both humans and dogs. In 2 patients, in whom platinum monopolar electrodes were implanted on the serosal surface of the antrum and a perfused manometric tube was placed in the stomach, the number of gastric contractions detected by manometry was only less than 50% of the pacesetter potentials accompanied by action potentials or second potentials. No contraction of the stomach was recorded by manometry when pacesetter potentials occurred without action potentials or second potentials. The relationship was further investigated in 11 anesthetized dogs prepared with implanted electrodes and sensitive ministrain gauges implanted on the serosal surface of the stomach and an intragastric manometric tube. In these dogs, phasic contractions were always recorded by the method using ministrain gauges although the electrical activity showed only PSPs without action potentials or second potentials. The manometry, however, could not recognize these phasic contractions. When the stomach was stimulated by bethanechol infusion through the splenic artery, as in the human stomach, the manometry detected less than 50% of gastric contractions detected by the strain gauge recording. The gastric dysrhythmia including tachygastria, tachyarrhythmia, and bradygastria was induced in 10 dogs by epinephrine, 100 micrograms X kg-1 X h-1, infused via the splenic artery. During the period of gastric dysrhythmia, the phasic contractions disappeared and no contraction associated with action potential could be observed. The phasic contractions reappeared as long as the PSPs occurred regularly in a frequency of 4-5 cycles/min during either the control period or during the period of epinephrine infusion. The epinephrine-induced gastric dysrhythmia was blocked or reversed to normal pacesetter potentials by intraarterial infusion of phentolamine. Our study suggests the following: (1) the pacesetter potentials not only pace and direct gastric contraction, but they may also play a role in the genesis of phasic contractions of the stomach, and (2) gastric contractions detected by sensitive strain gauges are not always recorded by the intraluminal manometry and, thus, gastric dysrhythmia may not be detected by the manometry in humans.

Action Potentials↗
PubMed1984

Muscarine increases tyrosine 3-monooxygenase activity and phospholipid metabolism in the superior cervical ganglion of the rat.

Muscarinic agonists cause a stable activation of tyrosine 3-monooxygenase in the superior cervical ganglion and increase the incorporation of 32Pi into phospholipids in the ganglion. We have studied the relationship between muscarine-stimulated phospholipid turnover and the muscarine-induced activation of tyrosine 3-monooxygenase. Both effects of muscarine are apparent within 2 min of incubation, and both are essentially independent of extracellular Ca++. All concentrations of muscarine that increase dopa synthesis also stimulate phospholipid turnover. Bethanechol is less efficacious than muscarine in producing both of these effects. Lithium, which disrupts phospholipid metabolism, inhibits the muscarine-stimulated accumulation of dopa. Other agents which affect phospholipid metabolism, including phospholipase C and deoxycholate, also increase the synthesis of dopa in the ganglion. These data support the hypothesis that changes in phospholipid metabolism mediate the activation of tyrosine 3-monooxygenase by muscarinic agonists.

Animals↗
PubMed1983

Pirenzepine and exocrine secretions: a selective agent for gastric glands?

Nineteen healthy volunteers were studied to investigate whether or not muscarinic receptors of different exocrine glands could be distinguished from one another by the use of pirenzepine. A simultaneous evaluation of lacrimation, salivation and gastric secretion was carried out, bethanechol (80 micrograms/kg/hr) being used as a stimulant and pirenzepine (10 or 5 mg i.v.) as an inhibitor. Bethanechol increased salivation significantly and the volume of gastric juice, and non-significantly increased lacrimation and total acid output. Pirenzepine abolished the hypersecretion induced by bethanechol, and decreased the basal level of the exocrine secretions, to approximately the same extent. These experiments seem to demonstrate that if there is a difference among the muscarinic receptors of lacrimal, salivary and gastric oxyntic glands, pirenzepine is unable to discriminate them from one another, at least under the experimental conditions of this investigation.

Adult↗
PubMed1984

The effect of the calcium antagonist verapamil on gastric acid secretion in humans.

Studies on isolated gastric glands and parietal cells suggest that calcium plays a role in the stimulus-secretion coupling of acid secretion. To determine which stimulants of human gastric secretion depend on calcium-mediated receptors, the effect of the calcium antagonist verapamil on gastric secretion was studied. Gastric secretion was stimulated by intravenous infusion of 50 micrograms/kg/h bethanechol, 10 micrograms/kg/h impromidine, 0.5 micrograms/kg/h pentagastrin, 4 mg/kg/h Ca++, or by sham feeding. Each type of stimulation was tested twice in six healthy subjects, alone and together with verapamil. Verapamil was administered as an intravenous bolus of 200 micrograms/kg followed by an infusion of 150 micrograms/kg/h. Six subjects had 2 step tests in which 4 doses of pentagastrin were administered consecutively in increasing dosage. Pentagastrin was given either alone or superimposed on a verapamil bolus followed by an intravenous infusion. Verapamil left gastric secretion stimulated by bethanechol, impromidine, or sham feeding unaffected. During Ca++ infusion verapamil caused a significant drop in volume, but not acid output. Pentagastrin-stimulated acid and volume output were significantly inhibited by intravenous verapamil, the inhibition resembling an uncompetitive pattern. Pentagastrin-stimulated gastric secretion was also inhibited by the calcium antagonist diltiazem. The results confirm earlier reports that calcium is involved in the stimulus-secretion coupling of the human gastric mucosa. Calcium appears to mediate the stimulation of acid secretion by gastrin.

Adult↗
PubMed1984

Calcitonin gene-related peptide: potent peripheral inhibitor of gastric acid secretion in rats and dogs.

Calcitonin gene-related peptide is a 37-residue peptide recently characterized in central and peripheral nervous system. The pharmacologic or physiologic importance of this peptide is not known. We studied the effect of calcitonin gene-related peptide on exogenously stimulated gastric acid secretion (pentagastrin, histamine, bethanechol, and intracisternal thyrotropin-releasing hormone) in the urethane-anesthetized rat. Calcitonin gene-related peptide (2.6 nmol/kg X h) caused a 63%-78% inhibition of gastric acid secretion with all secretagogues tested. The inhibition of gastric acid response to pentagastrin was dose-dependent (2.6-2630 pmol/kg X h), rapid in onset, quickly reversible upon cessation of calcitonin gene-related peptide infusion, and not modified by acute vagotomy or indomethacin pretreatment. In conscious dogs, gastric fistula acid response to pentagastrin was inhibited in a dose-dependent manner by calcitonin gene-related peptide (2.6-260 pmol/kg X h). The acid response of the Heidenhain pouch to pentagastrin was also inhibited by calcitonin gene-related peptide (260 pmol/kg X h). These results show that calcitonin gene-related peptide is a potent inhibitor of gastric acid secretion in the rat as well as in the dog. Its inhibitory action could be demonstrated against various stimuli and appears to be independent of prostaglandin or vagal pathways.

Animals↗
PubMed1984

Adrenergic influence on pentagastrin and bethanechol stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of alpha-, beta- and dopaminergic receptor stimulation and blockade on pentagastrin and bethanechol stimulated gastric acid secretion in conscious dogs with gastric fistula. Gastric acid secretion was found to be subject to a dose related inhibition by isoprenaline. The dose of isoprenaline producing approximately 50% inhibition was higher in the bethanechol--than the pentagastrin experiments (0.10 vs. 0.03 micrograms/kg/min.) and slightly lower after parietal cell vagotomy. The antisecretory effect was mediated via the beta 1-receptors alone. The inhibitory effect of isoprenaline on pentagastrin stimulated acid secretion showed the characteristics of competitive type and on bethanechol stimulated acid secretion of non competitive type. An increasing and dose-dependent stimulation of bethanechol stimulated gastric acid secretion was found for dopamine 1, 5 and 10 micrograms/kg/min. Dopamine (40 micrograms/kg/min.) exerted an inhibitory effect on pentagastrin and bethanechol stimulated gastric acid secretion mediated, via the beta 1-receptors. The stimulatory effect of low doses of dopamine during bethanechol stimulation could not be defined as an effect via beta-receptors. This dual response, the weak inhibitory effects and the potent decreasing effect on antral gastric motility indicate that dopamine has no physiologic relevant effect on gastric acid secretion. One may conclude that beta 1- and beta 2-receptors may exert an influence on gastric acid secretion in dogs. The main effect of dopamine seems to be on gastric motility, while the effect on gastric acid secretion is of minor importance.

Adrenergic beta-Agonists↗