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At least 289 records · Page 16Linked to original sources
PubMed1989

Characterization of substance P effects on sphincter of Oddi myoelectric activity.

We examined the effects of substance P (SP) on the myoelectric activity of the opossum sphincter of Oddi (SO). Myoelectric data from the SO in five adult opossums were recorded using thin stainless steel electrodes and computer-assisted analog-to-digital conversion. In fully awake and conscious animals, baseline spikeburst activity during phase I of the MMC occurred at a frequency of 28.6 +/- 3.1 spikebursts (SB) per 20-min period. Intravenous infusion of graded doses of substance P (from 0.5 to 8.0 micrograms/kg) stimulated SO myoelectric activity in a dose-related manner (from 80 +/- 8 to 235 +/- 11 SB/20 min, respectively, P less than 0.05 when compared to baseline). The effect of substance P on SO myoelectric activity was antagonized by administration of the H2-blocker, cimetidine (92.0 +/- 6.1 vs 48.2 +/- 7.0, n = 5, P less than 0.05). Administration of the antimuscarinic drug atropine only slightly affected the SO spikeburst frequency when infused prior to SP (73.0 +/- 10.4 vs 70.8 +/- 8.2, P greater than 0.05). We conclude that SP stimulated the SO spikeburst frequency in a dose-dependent fashion. Cimetidine markedly inhibited the response of the SO to SP but atropine did not. The excitatory effect of substance P on the opossum SO is mediated at least in part by a histaminergic, noncholinergic pathway.

Ampulla of Vater↗
PubMed1991

gamma-Aminobutyric acid and gastric acid secretion: a physiologic role?

The purpose of this study was to examine the effect of endogenous brain GABA levels or GABAergic tone on gastric acid secretion. Experiments were performed with Sprague-Dawley rats under urethane anesthesia. Continuous acid secretion was measured in vivo using a gastric luminal perfusion system. Initial experiments studied the effects on basal acid secretion of (aminooxy)acetic acid (AOAA), a substance which increases brain GABA levels, and flumazenil, a substance which decreases central GABAergic neurotransmission. After basal acid secretion was measured for 30 min, AOAA (15 mg/kg), flumazenil (10 mg/kg), or saline was given by intravenous infusion and acid secretion was measured for 120 min. There was no significant difference in acid secretion between groups (n = 8/group). A second series of experiments measured the effects of AOAA, flumazenil, or saline on gastric secretion during submaximal stimulation by bethanechol (180 micrograms/kg/hr) in normal and vagotomized rats. Total acid secretions (mean +/- SE) after saline, AOAA, or flumazenil were 78.7 +/- 11.8, 51.0 +/- 5.9, and 109.3 +/- 1.5 mumole/90 min, respectively (P less than 0.01). In vagotomized rats, there were no significant differences in rates of acid secretion between groups. In summary, GABAergic tone did not effect basal acid secretion in anesthetized rats. However, during submaximal acid secretion, acid secretion decreased when brain GABA levels increased, and acid secretion increased when GABAergic neurotransmission was inhibited. We conclude that endogenous brain GABA levels may effect gastric acid secretion in rats, perhaps via inhibition of central-vagal tone.

Aminooxyacetic Acid↗
PubMed1982

The effect of dibutyryl cyclic guanosine monophosphate, a competitive antagonist to cholecystokinin-pancreozymin, on gastric acid secretion in the isolated mouse stomach.

Dibutyryl cyclic guanosine monophosphate (dbcGMP), a specific competitive inhibitor of the gastrin, cholecystokinin-pancreozymin (CCK-PZ) family of peptides in pancreas, gallbladder and ileum, had no effect on basal acid secretion in the isolated mouse stomach nor on secretion stimulated by bethanechol or histamine. Secretion evoked by low doses of pentagastrin were likewise unaffected by dbcGMP but responses to high doses of pentagastrin were augmented. CCK-PZ and glucagon each inhibited acid secretion evoked by pentagastrin. DbcGMP blocked CCK-PZ-mediated inhibition but was without effect on inhibition by glucagon. These observations suggest that in the gastric glands there exist two receptors with different affinities for gastrin and CCK-PZ which mediate excitation and inhibition respectively.

Animals↗
PubMed1982

Modulation of pancreatic muscarinic receptors by weaning.

We have investigated the effects of early and delayed weaning on the development of the rat pancreatic muscarinic receptors. Weaning after 12, 14 and 16 complete days resulted in significantly increased concentrations of muscarinic receptors. Milk feeding, as the exclusive source of food, from day 12 to 23, 25 or 28, was associated with slight non significant decreases in receptor concentration. In both instances, early or delayed weaning, the apparent KDs of (3H-QNB binding were not affected. It is suggested that early solid food intake can modulate rapidly the pancreatic muscarinic receptor population while exclusive milk feeding does not seem to influence the dynamic of the muscarinic receptor population.

Amylases↗
PubMed1983

Bombesin and calcitonin secretion by pulmonary carcinoma is modulated by cholinergic receptors.

Three established cell lines derived from human small cell carcinoma of the lung, and known to produce significant amounts of peptide hormones were used to evaluate the regulation of hormone secretion by cholinergic agonists. In two of the cell lines (DMS 53, DMS 153) acetylcholine chloride, bethanechol chloride, and carbamylcholine at the concentrations of 10(-3)M to 10(-5)M stimulated secretion of bombesin and calcitonin as measured by RIA. The third cell line, DMS 406, was not significantly stimulated. Inhibition of induced stimulation by the cholinergic antagonist atropine, but not hexamethonium, indicated the presence of muscarinic rather than the nicotinic type of cholinergic receptors on the stimulatable cells. These receptors appear to mediate hormone secretion comparably to normal endocrine cells.

Acetylcholine↗
PubMed1983

Central noradrenergic-cholinergic interaction in regulation of gastric acid secretion in rats.

Possible roles of noradrenaline (NA) and acetylcholine (ACh) within the lateral hypothalamic area (LHA) in regulation of gastric acid secretion were examined in urethane anesthetized rats. When NA 30 nmoles was given into the LHA, the gastric acid output decreased and this inhibitory effect of NA was potentiated in rats pretreated with reserpine (2 mg/kg, i.p., 20 hr). Even in a dose of 3 nmoles which was without effect in non-treated control animals, there was a remarkable decrease in acid output. In these reserpinized animals, ACh in a dose of 30 nmoles induced a remarkable increase in acid output, while in the controls this ACh-induced increase was observed only with a 10 times higher dose. In the rats not given reserpine, the cholinergic muscarinic agonist bethanechol (10 nmoles) increased the gastric acid output while nicotine (30 nmoles) was without effect. Therefore, in rats, the central noradrenergic inhibitory mechanisms related to regulation of gastric function may be present at the level of LHA as well as at the ala cinerea (area of the dorsal motor nucleus of vagi and the nucleus tractus solitarius). In addition, in the LHA, a cholinergic muscarinic mechanism which elevates gastric acid secretion may be antagonized by a noradrenergic inhibitory mechanism.

Acetylcholine↗
PubMed1988

Evidence for a direct and indirect action of leucine enkephalin at the feline ileocecal sphincter.

An in vitro whole organ bath preparation was used to examine the effects of leucine enkephalin on the cat ileocecal sphincter (ICS) intraluminal pressure and myoelectric activity. The bath allowed separation of the bathing media surrounding the ICS and the ileum. Leucine enkephalin (2 x 10(-7) M) when added to the ileal bathing medium caused a delayed increase in ICS spike activity and pressure which was blocked by tetrodotoxin (10(-5)M). In contrast, leucine enkephalin (2 x 10(-7)M) added directly to the ICS bathing medium caused an immediate spike-associated contractile response which was tetrodotoxin-resistant. Thus both an indirect and direct opiate action at the ICS was demonstrated.

Action Potentials↗
PubMed1988

A novel muscarinic receptor antagonist AF-DX 116 differentially blocks slow inhibitory and slow excitatory postsynaptic potentials in the rabbit sympathetic ganglia.

Muscarinic, slow postsynaptic potentials (s-epsp and s-ipsp) in the rabbit superior cervical ganglia were shown to be differentially depressed by a novel cardioselective M2-type antagonist AF-DX 116: it antagonized the s-ipsp with IC50 value of 1.5 X 10(-7) M, which is 16-fold more potent in depressing the s-ipsp than the s-epsp. A hyperpolarizing component in the biphasic potential changes induced by a muscarinic agonist, methacholine, was selectively eliminated by this antagonist. AF-DX 116 was thus shown to be an useful tool for discriminating the M2-type muscarinic responses from those of M1-type in the nervous system.

Action Potentials↗
PubMed1989

Inhibitory action of galanin on gastric acid secretion in pentobarbital-anesthetized rats.

The effects of galanin and two galanin fragments, GAL(9-29) and GAL(15-29), were studied for potential effects on pentagastrin- and bethanechol-stimulated gastric acid secretion in a pentobarbital-anesthetized rat experimental model. At a dose of 10 micrograms/kg/h, galanin potently inhibited pentagastrin-stimulated gastric acid secretion whereas inhibition of bethanechol-stimulated gastric acid secretion was not statistically significant. Simultaneous iv infusion of galanin and atropine did not affect the inhibitory action of the former. In similar experiments, a GAL(15-29) fragment was completely inactive whilst GAL(9-29) retained only about 5% potency. These results indicate that galanin probably induces its inhibitory effects by acting directly on the parietal cells rather than through a cholinergic pathway. They also demonstrate that the rat gastric acid inhibitory activity of galanin depends critically on the integrity of the first fourteen N-terminal amino acids.

Animals↗
PubMed1990

Acid secretagogue mechanisms of a GABA-mimetic (PCPGABA) in the anesthetized rat: effects of hypothermia.

The secretagogue action of lipophilic, GABA-mimetic, beta-(p-chlorophenyl)-gamma-aminobutyric acid (PCPGABA) was studied in the rat in relation to body temperature. PCPGABA (2 to 8 mg/kg s.c.) stimulated acid output in the urethane-anesthetized rat whose core temperature ranged between 28 to 30 degrees C. However, this stimulatory effect of PCPGABA totally disappeared in the same animal whose rectal temperature was maintained at the normal unanesthetized level (37-39 degrees C), whereas the acid secretory responses to histamine and bethanechol were not modified with the change in the thermoregulation. This suggests that the thermoregulation mechanisms are implicated in acid secretagogue action of centrally acting gastric stimulants.

Animals↗
PubMed1990

A possible coupling of postjunctional ATP release and transmitters' receptor stimulation in smooth muscles.

The nature of ATP release from mainly smooth muscles of guinea-pig was evaluated with KCl and agonists for different kinds of receptors. In ileal longitudinal muscles, amounts of net ATP release by ACh and bethanechol (1-10 microM) were much larger (about 10 fold) than that by other drugs, e.g., histamine, 5-hydroxytryptamine, prostaglandin-F2 alpha, substance P and bradykinin, including KC1, although differences between contractions of the tissue evoked by test drugs were approximately 1.5 times at most. The ATP release, as well as the contraction, evoked by ACh or bethanechol was markedly reduced by atropine (0.3 microM), thus, indicating primarily postjunctional release of ATP. The remarkable ATP release from vas deferens by norepinephrine (NE), but not by substance P, was abolished almost completely by prazosin (0.3 microM). Increases in intracellular Ca2+ and subsequent contraction in the ileal tissue were produced by ATP and these responses were fully antagonized by nifedipine (0.1 microM). These findings provide evidence that the drugs-stimulated ATP release from smooth muscles does not result from contractility of muscles, but is substantially elicited only by stimulation of neurotransmitter (NE or ACh) receptors, suggesting the existence of the receptor-stimulus-postjunctional ATP release coupling. The released ATP may contribute, in part, to the muscle contractility via increase of Ca2(+)-influx, presumably, in a manner related to the voltage-gated Ca2(+)-channels.

Acetylcholine↗
PubMed1994

Effects of 17 beta-estradiol on endothelium-dependent relaxation induced by acetylcholine in female rat aorta.

Estrogens have been postulated to play an important role in modulation of vascular responses to endogenous reactive substances. The effects of chronic in vivo treatment with 17 beta-estradiol on relaxant responses to acetylcholine were investigated in the rat aorta isolated from prepubertal female rats. The selectivity of effects of 17 beta-estradiol on acetylcholine-induced relaxation was evaluated using histamine, another endothelium-dependent relaxant in the rat aorta. 17 beta-Estradiol significantly enhanced endothelium-dependent relaxation induced by acetylcholine, but did not alter the vascular responses to acetylcholine in endothelium-denuded aortic rings isolated from prepubertal female rats. In contrast, 17 beta-estradiol did not change endothelium-dependent relaxation induced by histamine in endothelium-intact aortic rings. The results of the present study demonstrate that 17 beta-estradiol selectively enhances acetylcholine-induced endothelium-dependent relaxation in the rat aorta.

Acetylcholine↗
PubMed1979

Evaluation of the control of glucagon secretion by the parasympathetic nervous system in man.

To evaluate the influence of the parasympathetic nervous system on human glucagon secretion, we have measured the plasma immunoreactive glucagon (IRG) levels after the administration of edrophonium, bethanechol chloride, and 2-deoxyglucose, and have compared the IRG responses to hypoglycemia in normal, atropinized, and vagotomized man. Edrophonium administered i.v. and bethanechol chloride administered s.c. did not affect IRG levels. Two-deoxy-glucose resulted in symptomatic neuroglucopenia with resultant vagal discharge, as evidenced by increased gastric acid secretion; but no changes in IRG concentrations were observed. The IRG response to insulin-induced hypoglycemia in normal subjects was not influenced by the administration of atropine. In seven subjects with a truncal vagotomy and no increased gastric acid secretion during insulin-induced hypoglycemia, the IRG increases were indistinguishable from those of control subjects in terms of timing, peak level obtained, or total glucagon response. We conclude that the cholinergic system is unlikely to play an important role in modulating glucagon secretion in man.

Adult↗