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PubMed1991

Cumulative dose-response curves for bethanechol-induced electrogenic secretion in rat jejunum in vitro: is tachyphylaxis a significant factor?

Electrogenic secretion was monitored as the short-circuit current (Isc) by an automatic voltage clamp across the isolated rat jejunum incubated in vitro. Responses to consecutive additions of bethanechol (1 mM) to the serosal surface showed tachyphylaxis. Addition of prostaglandin E2, however, after a single dose of 1 mM-bethanechol, induced an undiminished Isc response indicating that the tachyphylaxis was homologous. Dose-response curves for serosal applications of bethanechol obtained by serial-cumulative addition did not show tachyphylaxis when compared with those from a non-cumulative technique. The method of automatically recording the intestinal Isc with serial-cumulative addition of a serosal secretagogue gives dose-response curves free from tachyphylaxis.

Animals↗
PubMed1992

Enhanced electrogenic secretion in vitro by small intestine from glucagon-treated rats: implications for the diarrhoea of starvation.

Glucagon treatment of fed rats (50 micrograms I.P. every 6 h for 3 days) induces significant increases in vitro of the basal short-circuit currents of the jejunum (52%) and proximal ileum (81%) and in their electrogenic secretory responses to stimulation by bethanechol, a muscarinic agonist. The results support a role for glucagon in the intestinal hypersecretion observed in starvation and nutrient deprivation.

Animals↗
PubMed1966

Pharmacological properties of cholinoceptive neurones in the medulla and pons of the cat.

1. Iontophoretic application of acetylcholine to neurones in the medulla and pons of the unanaesthetized decerebrate cat excited 35.5% and inhibited 22%. This was not a representative sample of lower brain stem neurones, since most penetrations were made medially. Some cholinoceptive neurones were in the medial reticular formation.2. The time course of the response to different doses has been described.3. Nicotine and nicotinic agents 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) and choline phenyl ether (TM1) excited neurones excited by acetylcholine but, with one exception, did not inhibit neurones inhibited by acetylcholine.4. Muscarinic agents mimicked both the excitatory and inhibitory responses to acetylcholine. (+/-)-muscarine and bethanechol (beta-methylcholine carbamate) had a prolonged and powerful inhibitory action.5. Oxotremorine [1-(2-oxopyrrolidino)-4-pyrrolidino-butyne-2] had a long-lasting excitatory action on neurones excited by acetylcholine.6. Eserine and neostigmine potentiated the action of acetylcholine but in addition they had a strong excitatory effect on many brain stem neurones, independently of the action of acetylcholine.7. Excitatory and inhibitory responses to acetylcholine could be antagonized by gallamine, hexamethonium and atropine. Dihydro-beta-erythroidine (DHbetaE) antagonized only excitatory responses. (+)-Tubocurarine was a weak antagonist.8. It is concluded that the excitatory responses have both nicotinic and muscarinic properties but the inhibitory responses are only muscarinic. Since the pharmacology of these two types of response is different, it is concluded that the inhibitory action is not due to an indirect effect from excitation of a neighbouring inhibitory neurone.

Acetylcholine↗
PubMed1974

Concomitant changes in formaldehyde-induced fluorescence of dopamine interneurones and in slow inhibitory post-synaptic potentials of the rabbit superior cervical ganglion, induced by stimulation of the preganglionic nerve or by a muscarinic agent.

1. Dopamine was identified by formaldehyde histochemistry and cytospectrofluorometry in the rabbit's superior cervical ganglion. Dopamine was localized to the intraganglionic ;small intensely fluorescent' cells, and also to the characteristically beaded fibres forming a network in close contact with virtually all ganglion cell bodies. The extensive beaded fibres are therefore presumed to be processes of the small intensely fluorescent cells.2. Changes in the dopamine content of these interneurones were studied by recording alterations in their relative fluorescence intensity in conjunction with changes in the slow inhibitory post-synaptic potential (s.-i.p.s.p.) response of the ganglion to orthodromic nerve input.3. Dopamine content was lower after several hours in vitro even without special stimulation; this was in accord with a regularly observed spontaneous reduction of the s.-i.p.s.p. response.4. After a period of conditioning stimulation of the preganglionic nerve, in the presence of an anticholinesterase agent (eserine) and an inhibitor of catecholamine synthesis (alpha-methyl-p-tyrosine), the s.-i.p.s.p. was selectively and markedly reduced. The dopamine fluorescence in the small intensely fluorescent cell interneurones was also significantly reduced, to a mean value of about 55 or 60% of the fluorescence in the dopamine interneurones of the paired but unstimulated control ganglion. A significant reduction in dopamine fluorescence was always accompanied by a marked loss of s.-i.p.s.p. response; the reverse was not always true.5. Treatment with the muscarinic agent bethanechol for 30 min, with no alpha-methyl-p-tyrosine or eserine present, similarly resulted in reductions in the s.-i.p.s.p. response of the ganglia and in the formaldehyde-induced fluorescence of the dopamine interneurones.6. A functional uptake of extrinsic dopamine by the dopamine interneurones was also demonstrated: temporary exposure to dopamine restored a large fraction of both the s.-i.p.s.p. response and the dopamine fluorescence of the small intensely fluorescent cells, in ganglia already subjected either to the conditioning stimulation of the preganglionic nerve or to the action of bethanechol.7. It is concluded that (a) preganglionic impulses, by a cholinergic muscarinic synaptic action, can induce a release of dopamine from dopamine interneurones (small intensely fluorescent cells) in the superior cervical ganglion, (b) the ability of the ganglion to respond with a s.-i.p.s.p. to orthodromic input may be viewed as being dependent on the supply of functionally releasable dopamine in these interneurones, (c) the functionally releasable transmitter in vitro appears to comprise roughly 50% of the total dopamine content of the interneurones, and (d) the results fulfil some of the requirements of the hypothesis that a dopamine interneurone is activated muscarinically by preganglionic nerve impulses and mediates the production of s.-i.p.s.p. in sympathetic ganglion cells.

Action Potentials↗
PubMed1974

Pancreatic acinar cells: effects of lanthanum ions on amylase release and calcium ion fluxes.

1. The effect of La(3+) on amylase release and Ca(2+) fluxes in mouse pancreatic fragments in vitro was studied.2. Amylase release was increased by 0.1 mM-La(3+) and progressively inhibited by 1.0-10 mM-La(3+). Non-stimulated and bethanecol stimulated secretion were altered in an identical manner. Inhibition of amylase release was rapid and reversible.3. Uptake of (45)Ca(2+) was multiphasic with equilibrium with stable Ca(2+) still not complete after 2 hr. La(3+) (10 mM) limited uptake of (45)Ca(2+) to the extracellular space and slightly decreased total Ca(2+) content. Lower concentrations of La(3+) affected (45)Ca(2+) uptake and total Ca(2+) content in a biphasic manner which paralleled effects on amylase release.4. La(3+) restricted washout of (45)Ca(2+) to isotope in the extracellular space and abolished the bethanecol-stimulated increase in (45)Ca(2+) efflux.5. Uptake of (45)Ca(2+) into intracellular space, as measured by the ;lanthanum' method, was not affected by bethanecol.6. Tissue ultrastructure and Na(+) and K(+) content were not affected by La(3+).7. It is concluded that an influx of extracellular Ca(2+) is not important for triggering of secretion and that La(3+) may inhibit amylase release by acting on the release process rather than on Ca(2+) influx.

Amylases↗
PubMed1975

Chemical stimulatory mechanism in gastric secretion.

1. The serum gastrin level, gastric mucosal blood flow and acid secretion from the canine Heidenhain pouch have been measured in response to the introduction of bovine serum albumin, pepsin-digested albumin, an amino acid mixture, liver extract and mannitol used as control. 2. Distention of the Heidenhain pouch with mannitol or albumnin at pH 5-0 produced a similar pressure-related increase of acid secretion reaching a peak of only 10 percent of the maximal response to histamine. Pepsin-digested albumin was capable of producing larger acid outputs than undigested albumin. The highest acid output, attaining about 80 percent of the maximal response to histamine, was obtained with liver extract both before and after exhaustive dialysis to remove all the amino acids and short peptide fragments. An amino acid mixture containing all essential amino acids was also found to stimulate acid secretion but a lesser degree than liver extract. 3. This concluded that it is not the intact protein but the products of its digestion, the polypeptides and free amino acids, which are potent chemical stimulants of acid secretion from the oxyntic gland area. Since the serum gastrin level was not changed during acid secretion induced by peptic digests bathing the oxyntic gland area, the mechanism of chemical stimulation appears to be gastrin-independent. 4. The response to chemical stimulation by peptic digests can be greatly potentiated by combining this with distention of the oxyntic gland area. Topical application of xylocaine or atropine causes a marked decrease of Heidenhain pouch response to peptic digests, suggesting a possible neural reflex component in the mechanism of chemical stimulation of the oxyntic gland area. 5. When the pH of the liver extract in the Heidenhain pouch was gradually decreased in sequential order from 5-0 to 1-0, this resulted in a pH-related decrease in acid secretion and in the mucosal blood flow falling to the basal level at pH 1-0. Exogenous secretion given in graded doses from 0-5 to 8-0 u./kg. hr caused a small but dose-related inhibition of acid response to liver extract accompanied by a decrease of mucosal blood flow but without any significant change in the serum gastrin level. 6. The results indicate that the chemical stimulation of the oxyntic gland area by peptic digests is capable of inducing acid secretion by a local, gastrin-independent, partially neural reflex mechanism; sensitive to pH, pressure and secretin.

Albumins↗
PubMed1977

Effects of the calcium ionophore A23187 on pancreatic acinar cell membrane potentials and amylase release.

1. The effects of the Ca2+-ionophore A23187 and the non-metabolizable cholinergic agonist bethanechol on acinar cell membrane potentials and amylase release from the superfused mouse pancreas were studied. 2. In the presence of extracellular Ca2+ (2.56 mM), A23187 (10(-5)M) and bethanechol (3 X 10(-5)M) caused an equal increase in the release of amylase. Both stimulants depolarized theacinar cells, A23187 by 6-0 mV and bethanechol by 12-3 mV. 3. When Ca2+ and Mg2+ were removed from the superfusate, the ability of A23187 to increase the rate of amylase release was virtually abolished, while the effect of bethanechol remained unaltered. Similarly, in the absence of these divalent cations, A23187 did not cause depolarization of the acinar cells, while depolarization in response to bethanechol was largely normal. Consequently it is unlikely that cholinergic agonists initiate secretion by activating a Ca2+-ionophore-like mechanism in the cell membrane. 4. When the concentration of Ca2+ in the medium was raised to 10 mM was the only extracellular divalent cation present, the depolarization in response to A23187 was increased to 11-8 mV. When Mg2+ in a concentration of 10 mM was the only extracellular divalent cation, the depolarization was only 2-1 mV. 5. The Ca2+ dependent, A23187-induced depolarization was abolished in the absence of Na+ (Tris substitution). Addition of Na+ to the superfusate caused an immediate depolarization. 6. It is concluded that the Ca2+ dependent depolarization of pancreatic acinar cells induced by A23187 is not directly due to an increased divalent cation conductance. Our findings are consistent with the view that the depolarization is due to an increased influx of Na+ resulting from a Ca2+ mediated increase in Na+ permeability.

Amylases↗
PubMed1977

Synaptic excitation and inhibition resulting from direct action of acetylcholine on two types of chemoreceptors on individual amphibian parasympathetic neurones.

1. Synaptic transmission was studied in visually identified parasympathetic ganglion cells that modulate the heart beat of the mudpuppy Necturus maculosus).2. The brief pulse of acetylcholine (ACh) released from terminals of the vagus nerve after each impulse can produce two distinct post-synaptic responses in individual principal cells of the ganglion: (i) within a milli-second of release, ACh generates a rapid and strong excitatory post-synaptic potential (e.p.s.p.) that normally initiates a post-synaptic impulse; (ii) this excitation is usually followed by a slow hyperpolarizing inhibitory post-synaptic potential (i.p.s.p.) that lasts for several seconds. The magnitude and time course of the i.p.s.p. depends on the frequency and number of vagal stimuli. When the hydrolysis of ACh is inhibited by prostigmine, a train of nerve stimuli may be followed by an i.p.s.p. lasting half a minute or longer.3. The rapid e.p.s.p. and slow i.p.s.p. result from the direct action of ACh on two different types of chemoreceptors in the post-synaptic membrane of the principal cell. The e.p.s.p. can be preferentially blocked by the nicotinic antagonist dihydro-beta-erythroidine (5 x 10(-7)M), while the i.p.s.p. is selectively blocked by the muscarinic antagonist atropine (5 x 10(-9)M).4. Potentials resembling nerve-evoked e.p.s.p.s and i.p.s.p.s can be produced by iontophoretic release of ACh from micropipettes onto the post-synaptic membrane. Application of the muscarinic agonist bethanechol generates exclusively inhibitory responses.5. The reversal potential for the i.p.s.p. is about -105 mV, which is approximately the equilibrium potential for potassium (E(K)). When the external K(+) concentration is altered, the reversal potential for inhibition is shifted to the new value of E(K) as expected from the Nernst equation. Changes in the external Na(+) and Cl(-) concentrations have no appreciable effect on the reversal potential. Thus, the i.p.s.p. is the result of a conductance increase for K(+).6. The conductance change producing the i.p.s.p. is voltage sensitive. When the membrane potential is shifted from -40 to -60 mV, the i.p.s.p becomes larger and longer. Beyond -60 mV the inhibitory response decreases in proportion to the driving force on K(+) without any further change in time course.7. The inhibitory response produced by an iontophoretically applied pulse of bethanechol has a delayed onset of about 150 msec at 24 degrees C. The early portion of this response, including the delay, is proportional to t(3), where t is time. The proportionality factor (the apparent rate constant) decreases elevenfold when the temperature is lowered by 10 degrees C. This suggests that a multi-step process is involved in the activation of the conductance increase that leads to the inhibitory response. Inhibitory responses with similar kinetics were produced in heart muscles of the mudpuppy upon application of ACh.

Acetylcholine↗
PubMed1978

Inhibition by metiamide of secretagogue-induced gastric acid secretion in the conscious Heidenhain pouch rat.

1. The inhibition by metiamide of gastric of gastric acid secretion in response to histamine, pentagastrin and bethanechol has been investigated in the conscious Heidenhain pouch rat. 2. Histamine alone stimulated only a low rate of acid secretion. This response was markedly potentiated in the presence of mepyramine. 3. Metiamide at a dose of 0.15 mumole . kg-1 . min-1 I.V. significantly inhibited the acid secretory responses to histamine (in the presence of mepyramine) and pentagastrin. In each case the inhibition of acid output was the result of a significant decrease in both secretory volume and acid concentration. 4. Metiamide at a dose of 0.15 mumole . kg-1 . min-1 I.V. did not inhibit bethanechol-stimulated acid secretion. Increasing the dose of metiamide to 1.0 mumole . kg 1 . min-1 I.V. did produce a significant inhibition. In contrast with histamine and pentagastrin, metiamide inhibited bethanechol-stimulated secretion only by reducing acid concentration; there was no significant decrease in the gastric secretory volume. 5. It is concluded that these results are consistent with the view that histamine and pentagastrin share a common pathway in stimulating gastric acid secretion in the rat. The role of histamine in the control of bethanechol-stimulated acid secretion remains unclear.

Animals↗
PubMed1982

Role of cyclic adenosine monophosphate in amylase release from dissociated rat pancreatic acini.

1. The effect of octapeptide of cholecystokinin-pancreozymin (CCK(8)), bethanechol, cholera toxin, glucagon and vasoactive intestinal polypeptide (VIP) on amylase secretion and lactic dehydrogenase (LDH) release from isolated rat pancreatic acini was studied.2. In isolated rat pancreatic acini, in the absence of theophylline in the medium, amylase secretion was increased by 65-78% with 10(-7) and 10(-6) M-cholera toxin. In the presence of theophylline, amylase secretion was increased by 43-56% with 10(-7) and 10(-6) M-cholera toxin following a 90 min incubation. No effect was observed in the presence of theophylline at 30 and 60 min. The effect of cholera toxin was potentiated by CCK(8) at 60 and 90 min.3. In the absence of theophylline in the medium, amylase secretion was increased by 81-118% with 10(-5) and 10(-4) M-glucagon and 86% with 10(-6) M-VIP at 60 min. In the presence of theophylline in the medium, amylase secretion was increased by 53-246% with 10(-9) to 10(-6) M-glucagon and 111-158% with 10(-7) and 10(-6) M-VIP respectively. The effect of glucagon and VIP was potentiated by CCK(8).4. Potentiation of the rate of amylase release due to glucagon (10(-5) M) and VIP (10(-6) M) occurred during the first 15 min of incubation.5. Release of LDH was not increased by any of these agents.6. It is concluded that cyclic AMP rise (due to cholera toxin, glucagon and VIP effect) increased amylase secretion from rat pancreatic acinar cells. This effect is less marked than in the guinea-pig pancreas and is potentiated by agents mobilizing cellular Ca(2+) (CCK(8) and bethanechol).7. These data indicate species-specific variation in the action of cyclic AMP in the pancreas.

Amylases↗
PubMed1983

Peptidergic and muscarinic excitation at amphibian sympathetic synapses.

A single-electrode voltage clamp was used to study the slow muscarinic and late slow peptidergic excitatory post-synaptic currents (e.p.s.c.s) in B cells of the paravertebral sympathetic ganglia of the bull-frog. Conductance decreases were measured during peptidergic e.p.s.c.s in nearly all cells at clamped potentials near the resting level. In about half of the cells the size of the peptidergic e.p.s.c.s increased with hyperpolarization and in some of these cells conductance increases were found at hyperpolarized levels. In the remaining cells conductance decreases occurred at all levels of membrane potential tested, and in a few of these the polarity of the e.p.s.c.s reversed at hyperpolarized potentials. A similar diversity was observed among muscarinic e.p.s.c.s. At least two simple ionic mechanisms are required to explain the heterogeneous voltage dependencies observed: a conductance decrease primarily to K+ that dominates at depolarized potentials and a conductance increase to other ions that is more prominent at hyperpolarized potentials. The proportion of these two mechanisms appears to differ among B cells. The two slow e.p.s.c.s recorded in the same neurone had the same voltage dependence and were accompanied by the same conductance changes in each of eight cells despite differences between cells. The muscarinic e.p.s.c. was reduced during the peptidergic e.p.s.c. in each of twenty-five neurones tested over a range of membrane potentials. Externally-applied luteinizing hormone releasing hormone (LHRH) produced currents with the same voltage dependence and conductance changes as the nerve-evoked peptidergic e.p.s.c. in each of fifteen cells tested. Bethanechol, a muscarinic agonist, and LHRH produced currents with the same voltage dependence and conductance changes in each of the twelve cells studied. In several cells a saturating response to a prolonged application of LHRH completely occluded the response to bethanechol, and vice versa. Slow currents were recorded from dissociated cell bodies in response to bethanechol and LHRH; these responses exhibited the same diversity of voltage dependence and conductance changes as was observed in intact ganglia. Activation of muscarinic and peptidergic receptors may control shared ionic mechanisms in single ganglion cells.

Animals↗
PubMed1986

Characteristics of phasic and tonic sympathetic ganglion cells of the guinea-pig.

Intracellular recording techniques have been used to determine the electrophysiological properties of sympathetic neurones in ganglia of the caudal lumbar sympathetic chain (l.s.c.) and in the distal lobes of inferior mesenteric ganglia (i.m.g.) isolated from guinea-pigs. Passage of suprathreshold depolarizing current initiated transient bursts of action potentials in 97% of l.s.c. neurones, but only 13% of i.m.g. cells ('phasic' neurones). Most i.m.g. neurones fired continuously during prolonged depolarizing pulses ('tonic' neurones). Passive membrane properties varied; mean cell input resistance was similar between groups, but phasic neurones had smaller major input time constants on average than had tonic cells. Current-voltage relations determined under both current clamp and voltage clamp were linear around resting membrane potential (approximately 60 mV), where membrane conductance was lowest. Instantaneous and time-dependent rectification varied in the different neurone types. The current underlying the after-hyperpolarization following the action potential was significantly larger on average in tonic i.m.g. cells than in phasic neurones, although its time course (tau = 100 ms) was similar. Phasic neurones fired tonically when depolarized after adding the muscarinic agonist, bethanechol (10(-5) M to 10(-4) M), to the bathing solution. Bethanechol blocked a proportion of the maintained outward current (presumably the M-current, IM, Adams, Brown & Constanti, 1982) in phasic neurones; this current was small or absent in tonic neurones. Transient outward currents resembling the A-current (IA, Connor & Stevens, 1971 a) were evoked in tonic but not in phasic neurones by depolarization from resting membrane potential. IA could only be demonstrated in phasic neurones after a period of conditioning hyperpolarization. After a step depolarization to approximately --50 mV, IA reached peak amplitude at about 7 ms and then decayed with a time constant of about 25 ms in both neurone types. Activation characteristics of IA were similar for phasic and tonic neurones, but inactivation curves, although having the same shape, were shifted to more depolarized voltages in tonic neurones. That is, IA was largely inactivated at resting membrane potential in phasic, but not tonic neurones. It is concluded that the discharge patterns of the two populations of sympathetic neurones result from differences in the voltage-dependent potassium channels present in their membranes. The anatomical occurrence of the different cell types suggests that phasic neurones are vasoconstrictor and tonic neurones are involved with visceral motility.

4-Aminopyridine↗
PubMed1987

Importance of vagal input in maintaining gastric tone in the dog.

1. Using a gastric barostat to quantify variations in gastric tone, we had previously demonstrated that food ingestion or intestinal nutrient perfusion induces gastric relaxation. These data suggested a basal tonic contraction of the stomach during fasting. 2. To determine the role of vagal input in maintaining fasting gastric tone, we prepared two chronic canine models, either isolating both cervical vagal trunks in a cutaneous tunnel or including the supradiaphragmatic vagi within an implanted cooling jacket. In the fasted conscious dogs, we then studied the effect, on gastric tone, of acute and reversible vagal blockade by cooling. 3. Cervical vagal cooling produced a reversible gastric relaxation and increased the heart rate. Supradiaphragmatic vagal cooling produced a similar gastric relaxation without the cardiac effect. 4. Adrenergic blockade did not change either the base-line gastric tone or the cooling-induced relaxation. Adrenaline decreased gastric tone, but vagal cooling still produced a significant relaxation. 5. Atropine alone or combined with adrenergic antagonists produced a gastric relaxation that was not further increased by vagal cooling. Bethanechol increased gastric tone, an effect unchanged by vagal cooling. 6. We conclude that gastric tone during fasting is maintained by a cholinergic input, which is vagally mediated at both the cervical and the supradiaphragmatic levels.

Animals↗
PubMed1990

Intracellular recording from neurones of the guinea-pig gall-bladder.

1. Intracellular recordings were made from neurones of the guinea-pig gall-bladder in vitro. Intracellular injection of horseradish peroxidase revealed a simple structure, consisting of a soma and a single process, but no discernible dendritic arborization. 2. The resting membrane potential was -50.5 +/- 0.4 mV and the input resistance was 80 M omega. 3. Gall-bladder neurones spiked only once at the onset of depolarizing current pulses. Action potentials were blocked by tetrodotoxin, but a Ca2(+)-dependent spike could be elicited in the presence of tetrodotoxin and tetraethylammonium. 4. Action potential after-hyperpolarizations had a duration of 172 +/- 3.7 ms and reversed at a membrane potential of -93 mV; this reversal potential was linearly related to the logarithm of the external potassium concentration. The initial phase of the after-hyperpolarization was inhibited by tetraethylammonium (1-10 mM) and was not affected by 3,4-diaminopyridine. The late phase of the after-hyperpolarization was blocked by apamin (10 nM) or curare (500 microM). Both the early and late phases of the after-hyperpolarization were inhibited when the preparation was perfused with a calcium-free, high-magnesium solution. The calcium-free, high-magnesium solution had no effect on the membrane potential or input resistance of these cells. 5. Fast excitatory synaptic responses and antidromic responses were elicited in gall-bladder neurones by focal stimulation of fibre tracts. High-frequency fibre tract stimulation often resulted in prolonged, calcium-dependent, depolarizations that were associated with a decrease in input resistance. 6. 5-Hydroxytryptamine and substance P caused depolarizations that were associated with a decrease in input resistance. Bethanechol caused hyperpolarizations that were associated with a decrease in input resistance and which were blocked by atropine.

4-Aminopyridine↗
PubMed1982

Ontogeny of gastric acid secretion in the rat: evidence for multiple response systems.

Gastric acid secretion has been thought to depend on histamine stimulation of the parietal cell. However, in the 2-week-old rat neither exogenous histamine nor the H-2 receptor agonist impromidine stimulates acid secretion, whereas pentagastrin and the cholinergic agent bethanechol are potent stimuli. At this age, the effect of pentagastrin in acid secretion is not blocked by the H-2 receptor antagonist cimetidine, nor is it potentiated by impromidine. These data suggest that, in the rat pup, the acid secretory response to pentagastrin and cholinergic agents occurs before the histamine-mediated system is functional and operates independently of the actions of histamine.

Aging↗
PubMed1969

Oesophageal manometric studies in patients with chronic Chagas disease and megacolon.

Intraluminal manometric studies performed on 12 patients with chronic Chagas disease and megacolon without clinical or radiological abnormalities of the oesophagus showed no alteration in oesophageal physiology under basal conditions when compared with a control group of 30 healthy subjects. Oesophageal peristalsis was unimpaired. Patients with chronic Chagas disease and megacolon differed from normals in their reaction to a small dose of a cholinergic drug. This agent induced an isolated but significant increase in resting pressure at the level of the oesophagogastric sphincter, accompanied in most cases by an increase in spontaneous activity but not by a change in resting pressure in the body of the oesophagus. This is interpreted as a subclinical expression of oesophageal pathology related to Chagas disease.

Adult↗