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At least 649 records · Page 36Linked to original sources
PubMed1977

Biochemical reactions involved in pancreatic enzyme secretion. 2. Inhibitory effects of tetracaine and atropine.

Pancreatic enzyme secretion induced by urecholine or cholecystokinin-pancreozymin (CCK-PZ) is inhibited by tetracaine. If the pancreatic tissue is preincubated with tetracaine then washed out, the subsequent response to CCK-PZ is not affected while that to urecholine is impaired. In contrast with atropine, tetracaine loses its inhibitory potency once secretion has been initiated by urecholine before the addition of the local anaesthetic. Calcium efflux studies have shown that addition of tetracaine in vitro is associated with release of calcium in the incubation medium. This effect on calcium efflux might explain partly the inhibitory action of the drug.

Amylases↗
PubMed1977

Biochemical reactions involved in pancreatic enzyme secretion. 4. Effects of cytochalasin B on functions of the exocrine pancreas.

These experiments were performed to evaluate the effects of cytochalasin B on pancreatic enzyme secretion and thus perhaps establish a role for microfilaments in the exocytosis process. The alkaloid at a concentration of 1 microgram/ml (2micron) inhibits amylase secretion induced by urecholine or cholecystokinin-pancreozymin (CCK-PZ) but does not modify that induced by dibutyryl cyclic AMP. The inhibitory effect of the drug is reversible after a 30-min washing out period. It does not affect O2 consumption, basal calcium efflux, or efflux caused by CCK-PZ. Amino acid accumulation in the tissue and their incorporation into proteins are not modified. It is suggested that cytochalasin B inhibits pancreatic enzyme secretion, probably through an effect on the microfilament system.

Amylases↗
PubMed1982

Nonparallel transport of exportable proteins in rat pancreas in vitro.

The relative change in in vitro discharge of amylase (or total protein) versus pulse-labeled protein from rat pancreatic fragments was studied after in vivo stimulation with bethanechol or saline injections. Bethanechol was injection were pulse-labeled for 5 min with [14C]L-phenylalanine. The pulse was chased for 60 min. In fragments derived from animals injected with saline, ratio of amylase (or total protein) to new secretory protein decreased at 5 and 15 min but there was no change at 45 min of in vitro incubation with 5 X 10-5 M bethanechol. In fragments derived from animals injected with bethanechol, ratio of amylase to radiolabeled secretory protein decreased at 5 and 15 min and the ratio of total protein to radiolabeled secretory protein secretion decreased at 5 but not at 15 and 45 min. There was a lack of parallelism between the ratios of amylase to radiolabeled protein secretion and total protein secretion to radiolabeled protein secretion in animals injected with bethanechol in vivo followed by in vitro incubations. These experiments indicate that the older proteins are preferentially secreted under nonstimulated conditions and mixing of granules occurs following stimulation. The time required for mixing varies depending on whether the cells are stimulated or not. These data provide support for the concept that there may be more than one subpopulation of zymogen granules in the acinar cell leading to nonparallel enzyme secretion.

Amylases↗
PubMed1982

Trophic effects of chronic bethanechol on pancreas, stomach, and duodenum in rats.

Rats received a daily injection of 2, 6, or 12 mg kg-1 bethanechol for 7 or 14 days. Pancreatic weight and content of protein, amylase, and chymotrypsinogen were increased in a dose and time dependent fashion by bethanechol. After 14 days of treatment with the highest dose, pancreatic weight and total pancreatic DNA content increased to 1.18 times control (P less than 0.05) while protein increased to 1.25, amylase to 1.85, and chymotrypsinogen to 1.72 times control. There was a slight increase in oxyntic gland area weight in bethanechol-treated rats, but content of DNA, protein, and pepsinogen were not changed. Bethanechol had no effect on duodenal weight or content of DNA, protein, or maltase. Acute administration of 12 mg kg-1 bethanechol increased circulating gastrin levels for at least 4 h in unanesthetized rats. We conclude that long-term treatment with a cholinergic agonist produces pancreatic hyperplasia and increases protein and enzyme content. Under the conditions of this study, no effects were seen on oxyntic gland area of stomach or duodenum.

Animals↗
PubMed1985

The distension stimulus to gastric acid secretion in the isolated mouse stomach.

Distension of the isolated mouse stomach stimulated gastric acid secretion. Atropine, cimetidine, or proglumide antagonized the actions of cholinomimetics, histamine, and gastrin, respectively. However, these antagonists and the nerve blocking agent, tetrodotoxin, were without effect on basal secretion or distension-stimulated secretion. It is concluded that in the isolated mouse stomach neither basal secretion nor secretion evoked by distension involve the release of any of the established "physiological" secretagogues or the activation of intramural nerves.

Animals↗
PubMed1987

Vagal inhibition of gastric acid secretion: evidence for cholecystokinin as the inhibitory transmitter in the mouse stomach.

In the mouse isolated stomach preparation, electrical stimulation of vagal preganglionic fibres activated cholinergic excitatory pathways and noncholinergic inhibitory pathways to the gastric glands. Both were blocked by hexamethonium suggesting that there is at least one nicotinic synapse in each. The inhibitory vagal response was blocked by dibutyryl cyclic GMP, an established cholecystokinin antagonist which abolished cholecystokinin-mediated inhibition of acid secretion. It is suggested that there are direct inhibitory vagal pathways to the gastric glands and that cholecystokinin may be the inhibitory transmitter.

Animals↗
PubMed1988

Antiulcerogenic and antisecretory effects of a novel diphenylmethane derivative and antiestrogen binding site ligand.

N,N-Diethyl-2-[4-(phenylmethyl)-phenoxy]-ethanamine hydrochloride (DPPE) is a para-diphenylmethane derivative that binds selectively and with high affinity to the microsomal antiestrogen binding site (AEBS). Recent studies with DPPE indicate that AEBS is closely related to a lower affinity non-H1, non-H2 histamine site that may be associated with calcium channels; the DPPE-AEBS site is different from that which verapamil binds, however, DPPE, but not verapamil, demonstrates antiproliferative effects in vitro and is antiestrogenic in vivo. We now show that DPPE profoundly inhibits restraint and cold stress and ethanol-induced gastric ulcer formation, accelerates ulcer healing, attenuates the stress-induced rise in plasma corticosterone level, and significantly reduces basal and H2 agonist (dimaprit)-stimulated and, to a lesser extent, bethanechol-stimulated gastric acid output in conscious rats. A nonulcerogenic but prostaglandin-depleting dose of indomethacin completely blocks the inhibitory effects of DPPE on stress ulcer formation. Conversely, verapamil only slightly attenuates dimaprit-stimulated gastric acid secretion and exacerbates ethanol-induced gastric ulcers; its anti-stress ulcer effects are only partially attenuated by indomethacin. These findings support the likelihood that the site of action of DPPE is different from that of verapamil, and that an effect on prostaglandins may, at least in part, contribute to its antiulcer and apparent cytoprotective effects.

Animals↗
PubMed1992

Differential sensitivities of the sphincter of Oddi and gallbladder to cholecystokinin in the guinea pig: their role in transsphincteric bile flow.

Cholecystokinin (CCK) is considered to simply contract the gallbladder and relax the sphincter of Oddi with meals. In this study, we examined this hypothesis by investigating the action of CCK on the sphincter of Oddi and gallbladder of the guinea pig. The experimental design used an in vitro preparation of the sphincter of Oddi to measure contraction of the circular muscle. CCK increased tone in both the gallbladder and the sphincter of Oddi in a concentration-dependent manner. The normalized concentration-response curves for CCK, however, revealed that the gallbladder had a greater sensitivity to CCK (ED50 7 nM) than the sphincter of Oddi (ED50 22 nM; p < 0.01). Conversely, the sphincter was more sensitive to bethanechol than was the gallbladder. When the sphincter of Oddi was stimulated maximally with CCK in the presence of atropine (10(-6) M) or tetrodotoxin (10(-6) M), the contractile response was significantly reduced (p < 0.05) although not abolished. Conversely, atropine completely abolished the responses to bethanechol (10(-3) M) and transmural field stimulation (70 V, 10 Hz, 1 ms, for 20 s). Transmural field stimulation of the sphincter that had been precontracted with CCK (26 nM) caused a transient, initial relaxation followed by contraction. Pretreatment with atropine augmented the duration of this relaxation, which could be completely abolished by tetrodotoxin. Thus, CCK contracts the sphincter of Oddi in the guinea pig by a direct (myogenic) and a neural (likely cholinergic) mechanism. Relaxation of the sphincter of Oddi also occurs in the guinea pig via noncholinergic inhibitory nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Increased phosphate efflux from acinar cell during protein secretion.

The permeability of the pancreatic epithelium to two water soluble molecules, sucrose and inulin, increases when protein secretion is augmented by a cholinergic agonist. An increase in the permeability of passive paracellular shunts (3) has been proposed to account for these observations. In the present experiments we have measured the distribution of another molecule, phosphate ion, across the epithelium by following its secretion from the cannulated duct of whole-rabbit pancreas in short-term organ culture. A cholinergic stimulant increases phosphate ion concentration in secretion in a similar fashion to that seen for the watersoluble nonelectrolytes. However, both the unstimulated rate of phosphate secretion and the increase observed with cholinergic stimulation were not dependent on the presence of the ion in the medium, and therefore its secretion in both cases reflects phosphate efflux from the cell and not its paracellular transport. The results indicate that either the phosphate ion is excluded from paracellular shunts or that such shunts do not contribute substantially to the transpancreatic passage of molecules of this size.

Animals↗
PubMed1986

Neuropeptides degranulate serous cells of ferret tracheal glands.

To determine whether serous or mucous cells in tracheal submucosal glands respond to the neuropeptides substance P (SP) and vasoactive intestinal peptide (VIP), we studied the peptide-induced changes in gland cell morphology accompanying release of 35SO4-labeled macromolecules from tracheal explants of ferrets. Explants were labeled for 1 h in medium containing 35SO4 and washed for 3.5 additional hours. Base-line secretion in the absence of drugs declined between 1.5 and 3.5 h after the pulse. Between 2.5 and 3.5 h, the average percent change in counts per minute recovered per sample period was not significantly different from zero (P greater than 0.3; n = 6). Substance P (10(-5) M) and VIP (2 X 10(-6) M) added 4 h after labeling each increased greatly the release of 35SO4-labeled macromolecules (SP, 219%; VIP, 180%) above base line. Bethanechol, a muscarinic-cholinergic agonist (10(-5) M), increased secretion by an average of 142% above base line (each effect, P less than 0.05; n = 6 each). Light and electron microscopy of the control tissues showed glands with narrow lumens and numerous secretory granules. Glands treated with SP or VIP had enlarged lumens and the serous cells were markedly degranulated. These phenomena were documented by morphometry and suggest that SP and VIP cause secretion from glands at least partially by stimulating exocytosis from serous cells.

Animals↗
PubMed1990

Characterization of a muscarinic receptor controlling Cl- secretion in hen trachea.

We have attempted to characterize a muscarinic receptor subtype involved in Cl- secretion in isolated epithelium of hen trachea, taking advantage of drugs developed in the last 15 yr. Hen trachea can be stimulated to secrete Cl- equal to approximately 80-90 microA/cm2 by application of acetylcholine (ACh) to the serosal side. The process has an apparent dissociation constant (Kd) for ACh of 740 nM. The Cl- secretion is completely inhibited by 20 microM bumetanide at the serosal side. Of five selective antagonists for muscarinic receptors, pirenzepine, hexahydrosiladifenidol, dicyclomine, 11-([2-[(diethylamino)-methyl]-1-piperidinyl]acetyl)-5,11- dihydro-6H-pyrido(2,3-b)(1,4)benzodiazepine-6-one, and 4 diphenyl acetoxy-N-methylpiperidine methobromide, only the latter had a high affinity for the functional receptor with an apparent Kd of 3 nM. The receptor may be classified as an M4-muscarinic receptor subtype and probably belongs to a group of muscarinic receptors on exocrine glands and mucosal cells involved in ion transport. All the functional responses caused by muscarinic agonists and antagonists tested exhibited exponents (apparent Hill coefficients) in the range from 1.3 to 2.4, indicating a gain in the stimulus secretion coupling mechanism, an aspect of muscarinic receptor function that is not revealed in radioligand binding studies.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1977

Actions of cholecystokinin octapeptide on smooth muscle of isolated dog intestine.

Adult dogs were anesthetized and segments of small intestine were isolated and perfused via a mesenteric artery with Krebs-bicarbonate solution. Muscle responses along the circular and longitudinal axes were monitored with extraluminal strain gauge transducers. Agonists were administered as intraarterial bolus injections in volumes not exceeding 0.1 ml. Antagonists were dissolved in the Krebs perfusion solution. The C-terminal octapeptide of cholecystokinin (CCK-OP) produced dose-related tonic and phasic contractions of smooth muscle along the transverse axis and tonic and phasic relaxations along the longitudinal axis of the muscle segments. Smooth muscle responses to CCK-OP were reduced by atropine sulfate (0.1 mug/ml) and minimally affected by hexamethonium (10 mug/ml) perfusion. Tetrodotoxin (TTX, 5 ng/ml) selectively reduced muscle responses to dimethylphenylpiperazinium (0.5 mug) and CCK-OP (0.2 mug) but failed to alter responses to bethanechol (BeCh, 5 mug). Higher concentrations of TTX (10 ng/ml) abolished responses to CCK-OP. Depolarizing doses of nicotine (500 mug) selectively antagonized responses to 5-hydroxytryptamine (5HT, 5 mug) and CCK-OP (0.2 mug) but did not alter responses to BeCh (5 mug). Perfusion with tetraethylammonium (1 mg/ml) reduced muscle responses to depolarizing doses of nicotine and abolished the nicotine-induced antagonism of 5HT and CCK-OP. The intestinal smooth muscle response to CCK-OP in the dog is mediated through a neurogenic mechanism. CCK-OP interacts with a nonnicotinic receptor on postganglionic cholinergic neural elements in this preparation.

Animals↗
PubMed1978

Histaminergic pharmacology of primate lower esophageal sphincter.

We have studied the lower esophageal sphincter (LES) response to exogenous histamine and to H1- and H2-blocking agents in the awake baboon. Increasing intravenous bolus doses of histamine produce an increase in LES pressure with a maximum response at a dose of 12 microgram/kg. H1-receptor blockade with chlorpheniramine over a wide dose range did not alter basal LES pressure but did abolish the response of the LES to exogenous histamine. H2-receptor blockade with cimetidine at doses markedly inhibiting gastric acid secretion (2 mg/kg.h) did not alter basal LES pressure or the response of the LES to exogenous histamine. In addition, cimetidine did not alter the response of the LES to pentagastrin and bethanechol. Although histamine and histamine receptors are important in gastric secretion, they appear to have no identifiable role in the maintenance of basal LES smooth muscle tone in the baboon. These results demonstrate the presence of a stimulatory H1 receptor on baboon LES smooth muscle, but provide no evidence for the presence of an H2-inhibitory receptor. As opposed to the parietal cell, the LES response to pentagastrin and bethanechol does not require a H2 receptor.

Animals↗