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At least 145 records · Page 8Linked to original sources
PubMed1985

Protective effect by UCB JO28 against histamine and methacholine induced bronchial hyperreactivity.

UCB JO28 [( 2-[2-[4-(diphenylmethylene)-1-piperidinyl] ethoxy] ethoxy] acetic acid, hydrochloride) is derived from diphenylmethylene piperidine. Animal experiments have shown that it has spasmolytic properties for smooth muscle, particularly in the bronchi, as well as anti-Hl, anticholinergic and anti-serotonin activities. The degree of protection by JO28 against histamine and methacholine-induced bronchospasm has been investigated in 20 asthmatic patients with serious airways hyper-reactivity. Protection against histamine-induced bronchospasm was almost complete in 11 out of 12 patients, whereas protection against methacholine-induced bronchospasm, although clearly present in seven of eight patients, was less marked.

Adolescent↗
PubMed1989

Okadaic acid, a phosphatase inhibitor, produces a Ca2+ and calmodulin-independent contraction of smooth muscle.

The effects of okadaic acid, a phosphoprotein phosphatase inhibitor, on the contractile response and on myosin light chain phosphorylation were studied in intact lamb tracheal smooth muscle. The effects of okadaic acid were compared to the response of the same fibers stimulated with 1 microM methacholine, a concentration that induces 90% of maximal force. Okadaic acid (50 microM) produced a slow but maximal contraction that was accompanied by an increase in phosphorylation of the 20 kDa light chain of myosin. The myosin light chain phosphorylation pattern induced by okadaic acid, however, differed from that induced by methacholine. Ca2+ depletion, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin antagonist and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), a protein kinase C inhibitor, blocked or attenuated methacholine-induced contractions but had no significant effect on force development or myosin light chain phosphorylation induced by okadaic acid. These results suggest that phosphorylation of the 20 kDa light chain of myosin is essential for smooth muscle contraction; they also suggest that okadaic acid either uncovers or activates an apparently Ca2+ and calmodulin-independent protein kinase activity that phosphorylates the 20 kDa light chain of myosin at multiple sites.

Animals↗
PubMed1980

Augmented amylase release from rat parotid gland slices, in vitro.

Using a continuous amylase assay the effect of a simultaneous stimulation of adrenergic and cholinergic receptors on amylase release by perfused rat parotid slices was investigated. Superimposing adrenergic stimulation (isoprenaline) on continual submaximal cholinergic stimulation (acetyl-beta-methylcholine) resulted in an augmented amylase release compared with the sum of the two separate effects. This could also be shown with continual adrenergic stimulation with cholinergic stimulation superimposed on this. Possible explanations of this effect are discussed with particular respect to the role of Ca++.

Amylases↗
PubMed1986

Effect of methacholine on ionic permeability of basal membrane of the eccrine secretory cell.

In an attempt to clarify the possible change in ionic permeability of the basal membrane of secretory cells during methacholine (MCH) stimulation, the effect of ionic substitution on membrane potential (PD) was studied in the isolated monkey palm eccrine secretory tubule. The mean PD (Vcb) was -73 mV. Stimulation with local iontophoresis of MCH caused a biphasic change in Vcb, an initial transient depolarization of 5 to 10 mV, followed by repolarization near the resting PD. MCH-induced PD transient reversed its polarity at -43 mV (MCH-null potential). Vcb markedly depolarized by an increase in [K+]b or a decrease in [Cl-]b. Ion-dependent partial potential ratio (Ti) using the estimated change in electromotive force delta Eb yielded values of 0.72 for K+ and 0.26 for Cl-, indicating that the basal membrane is conductive predominantly to K+ and Cl-. However, delta Vcb due to K+ or Cl- replacement did not change before or during MCH stimulation. Although replacement of Na+ with Tris+ or Li+ transiently depolarized Vcb, the delta Vcb reversed to hyperpolarization during MCH stimulation, suggesting that MCH causes a small increase in Na+ conductance across the basal membrane. The implication of these data have been discussed within the conceptual framework of ionic movements in Cl- transporting epithelia.

Animals↗
PubMed1985

Characterization of the muscarinic receptor in human tracheal smooth muscle.

Muscarinic receptors in human tracheal smooth muscle were characterized by radioligand binding and functional studies. Specific [3H]-(-)-quinuclidinylbenzilate ([3H]-(-)-QNB) binding to tracheal smooth muscle membranes was reversible, stereoselective and of high affinity (Kd = 47 +/- 4 pmol/l; RT = 920 +/- 120 fmol/g tissue). Inhibition of specific [3H]-(-)-QNB binding by the M-1 selective antagonist pirenzepine was found to occur at relative high concentrations classifying the muscarinic receptor population as belonging to the M-2 subclass. Inhibition of specific [3H]-(-)-QNB binding by muscarinic agonists revealed the presence of high and low affinity sites in nearly equal proportions. 5'-Guanylylimidodiphosphate converted high affinity sites into low affinity sites although its effect was minimal. Log dose-contraction curves of methacholine had Hill coefficients of 1.10 +/- 0.04 with pD2-values of 6.75 +/- 0.02. Inhibition of specific [3H]-(-)-QNB binding by methacholine, however, was best described by a two binding site model with pKi-values considerably lower. The difference between these affinity values points to the presence of substantial receptor reserve.

Adolescent↗
PubMed1984

Factors related to gastric hypersecretion during pregnancy and lactation in rats.

We attempted to elucidate the factors involved in gastric hypersecretion of rats during pregnancy and lactation. Acid secretion in pylorus-ligated and vagally denervated fistula rats stimulated with histamine, tetragastrin, and methacholine increased from midterm pregnancy and persisted during lactation. Pepsin secretion remained unaltered during pregnancy but increased during lactation. Vagal denervation itself abolished this hypersecretion. In late pregnancy, a delayed appearance of maximal acid response to histamine was apparent, as compared to nonpregnant rats, and was abolished by aminoguanidine treatment. There was a delay in the maximal response to tetragastrin but not to methacholine. Serum histamine concentrations were 3-4 times higher in late pregnancy, as compared to nonpregnant, lactating and nonlactating rats. Gastric DNA and protein concentrations were significantly increased in lactating rats with concomitant elevation of food intake and serum gastrin levels. Those changes disappeared in nonlactating rats, and gastric secretion was much the same in the nonpregnant rats. These results indicate that acid hypersecretion during pregnancy was exclusively associated with vagal innervation plus high serum histamine levels, while acid and pepsin hypersecretion in lactating rats were associated with vagal innervation plus hyperplastic gastric mucosa and high serum gastrin levels.

Animals↗
PubMed1989

Electron probe X-ray microanalysis of cellular ions in the eccrine secretory coil cells during methacholine stimulation.

Intracellular concentrations of Na, K, Cl ([Na], [K] and [Cl], respectively) and other elements were determined in isolated monkey eccrine sweat secretory coil cells using quantitative electron probe X-ray microanalysis of freeze dried cryosections. The validity of the methodology was partially supported by qualitative agreement of the X-ray microanalysis data with those obtained by micro-titration with a helium glow spectrophotometer. [Na], [K] and [Cl] of the cytoplasm were the same as those in the nucleus in both clear and dark cells. [Na], [K], and [Cl] of the clear cells were also the same as those of the dark cells at rest and after stimulation with methacholine (MCh), suggesting that these two cell types behave like a functional syncytium. MCh stimulation induced a pharmacologically specific, dose-dependent decrease in [K] and [Cl] (as much as 65%), and a 3.7-fold increase in [Na]. In myoepithelial cells, a similar change in [Na] and [K] was noted after MCh stimulation although the decrease in [Cl] was only 20%. The MCh-induced change in [Na], [K] and [Cl] was almost completely inhibited by removal of Ca2+ from the medium. 10(-4) M bumetanide inhibited the MCh-induced increase in [Na], reduced the decrease in [K] by about 50%, but slightly augmented the MCh-induced decrease in [Cl]. 10(-4) M ouabain increased [Na] and decreased [K] as did MCh; however, unlike MCh, ouabain increased [Cl] by 56% after 30 min of incubation. Thus the data may be best interpreted to indicate that Ca-dependent K efflux and (perhaps also Ca-dependent) Cl efflux are the predominant initial ionic movement in muscarinic cholinergic stimulation of the eccrine sweat secretory coils and that the ouabain-sensitive Na pump plays an important role in maintenance of intracellular ions and sweat secretion.

Animals↗
PubMedDate not supplied

The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation.

The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed.

Acetylcholine↗
PubMed1988

Action of a novel drug (Zy 16039) on mucus secretion in the ferret isolated trachea in vitro.

1. The effect of 4-H-2-carboxamido-4-phenyl-thieno-[3,2c]-[1]-benzopyran (Zy 16039) was examined on the smooth muscle contraction, mucus secretion and albumin transudation in the ferret whole trachea in vitro. 2. Zy 16039 (0.1-20 microM) produced a concentration-dependent relaxation of the ferret trachea contracted by methacholine (1 microM) and phenylephrine (10 microM). The relaxations were about 20% of the full contractions. 3. Zy 16039 has no effect on the resting (zero) output of mucus in the ferret trachea. Methacholine-induced mucus secretion was significantly inhibited by Zy 16039, whereas phenylephrine-induced secretion was significantly increased. 4. Methacholine-induced secretion of lysozyme, a marker of serous cell secretion, was inhibited by Zy 16039 both with regard to output and concentration of lysozyme. In contrast, Zy 16039 significantly increased the output of lysozyme due to phenylephrine, with no effect on concentration. 5. Zy 16039 had no significant effect on the rate of output of fluorescent albumin through the tracheal wall. However the concentration of albumin in the mucus samples was changed because of the effect of Zy 16039 on mucus secretion induced by methacholine and phenylephrine. 6. We conclude that Zy 16039 relaxes airway smooth muscle, and either promotes or inhibits mucus secretion depending on its source. It has qualitatively similar actions to vasoactive intestinal peptide.

Albumins↗
PubMed1983

Effect of somatostatin, secretin, and glucagon on secretagogue stimulated aminopyrine uptake in isolated canine parietal cells.

Somatostatin, secretin, and glucagon have been shown to inhibit gastric acid secretion in vivo and thus have been postulated to act directly on the parietal cell. To test the hypothesis that these peptides directly influence the acid secretory cells, we studied the effect of the three gastrointestinal hormones using aminopyrine uptake as an index of acid production. The parietal cells were stimulated to increase aminopyrine uptake by submaximal concentrations of histamine (10(-6) mol/l), methacholine (10(-6) mol/l), and pentagastrin (10(-6) mol/l), but in no concentrations did these gastrointestinal hormones affect any of the secretagogues' response. Our data suggest that gastrointestinal peptides do not modulate acid secretion at the parietal cell level.

Aminopyrine↗
PubMed1984

On the mechanism of histamine-induced bronchodilation in conscious guinea-pigs.

The bronchodilatory effect of histamine was evaluated in a conscious guinea-pig model of cholinergically mediated bronchoconstriction. The H1, bronchoconstrictor, property of histamine was masked using high doses of the H1-antagonist chlorpheniramine (30 mg/kg), and the bronchodilatory activity evaluated by observing the increase in latency to collapse induced by aerosol methacholine. Under these conditions, histamine (1.0, 3.0 or 10.0 mg/kg, i.p.) delayed methacholine-induced collapse in a dose-dependent manner. Cimetidine, an H2-receptor antagonist (10 to 100 mg/kg), did not delay collapse either in the presence or absence of an H1-antagonist. However, when cimetidine was administered prior to histamine, the bronchodilatory activity of histamine was abolished. A similar abolition of histamine bronchodilation was observed if propranolol, a beta-adrenoceptor antagonist, was administered prior to histamine. Propranolol alone had no effect on methacholine-induced bronchospasm. These data suggest that the major bronchodilatory property of histamine may be mediated indirectly via catecholamine release through an H2-receptor mechanism.

Aerosols↗
PubMed1987

Pulmonary aerosol actions of LY188695 (KB2413), a new potent H1-receptor antagonist.

The new potent H1 receptor antagonist, LY188695 (KB2413), was delivered to guinea pigs as a pulmonary aerosol and its ability to inhibit histamine-induced airway obstruction examined. Aerosol LY188695 was more effective than inhaled chlorpheniramine or clemastine in reducing the pulmonary gas trapping produced by histamine challenge. Lung antihistamine effects occurred within minutes of a brief, low concentration aerosol exposure and persisted for at least 1 hour. LY188695 aerosol treatment did not produce significant inhibition of methacholine-induced gas trapping. Although systemic antihistamine effects occurred 50 minutes after LY188695 inhalation, aerosol administration produced an enhanced local (i.e., lung) action compared to intravenous delivery.

Aerosols↗
PubMed1981

Ro 21-7634, a new antiallergic agent with potent oral activity.

Ro 21-7634 was examined for oral antiallergic activity in two in vivo models commonly used to evaluate antiallergics. In the rat PCA test, this drug had an oral ID50 of 1.14 mg/kg and was found to be more potent than several other antiallergics including Disodium Cromoglycate (cromoglycate), Oxatomide, Doxanthrazole, Xanoxate, 2,6-bis (ethyoxyoxalylamino) pyridine, PRD-92-EA and M + B 22,948. In contrast to cromoglycate, Ro 21-7634 was found to be an orally active inhibitor of antigen-induced broncho-constriction in passively sensitized rats (ID50 = 0.2 mg/kg). In addition, Ro 21-7634 inhibited antigen-induced histamine release in an in vivo passive peritoneal anaphylaxis test system, following intraperitoneal administration. Ro 21-7634 demonstrated no end organ antagonism toward histamine, metacholine or serotonin in the guinea pig.

Administration, Oral↗
PubMed1987

Chronic idiopathic intestinal pseudo-obstruction caused by acquired visceral neuropathy localised in the left colon: report of two cases.

Two cases of chronic idiopathic intestinal pseudo-obstruction (CIIP) are reported. One is a 51-year-old man, and the other is a 47-year-old woman. Both patients presented with severe constipation and barium enema showed a marked dilation of the right colon, and a narrowing in the left colon. Studies done on the motility of the colon and anorectum revealed normal resting pressure profiles of the anorectom, a normal recto-anal reflex, and a normal resting tone of the collapsed colon. Administration of methacholine chloride, however, provoked large, non-propulsive movements in the collapsed colon, which were inhibited by the administration of atropin sulfate. Histologic examination disclosed a marked decrease in neurons and an increase of Schwann cells in the myenteric plexus of the collapsed colon. CIIP due to acquired visceral neuropathy localised in the left colon, was diagnosed as a result of manometric and histologic findings. One case was cured surgically, by a left hemi-colectomy, and the other was cured medically using choline antagonists and laxatives.

Chronic Disease↗