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At least 1,009 records · Page 56Linked to original sources
PubMed1975

Effect of carbacholine and urecholine on pentagastrin-stimulated gastric secretion in healthy subjects.

Dose-response studies of pentagastrin-stimulated gastric secretion were performed in 6 healthy volunteers. On different days pentagastrin was given in doses of 0.15, 1.5, and 15 mug/kg/hr either alone or in combination with carbacholine, 2 mug/kg/hr, or urecholine, 60 mug/kg/hr. Carbacholine and urecholine increased acid and pepsin secretion evoked by the lowest dose of pentagastrin while there was no augmentation at the highest dose. The dose of pentagastrin required to elicit half maximal acid output (Km) tended to decrease by simultaneous infusion of carbacholine or urecholine, suggesting that the cholinomimetics increased the sensitivity of the parietal cells to pentagastrin stimulation. Km for pentagastrin alone was higher than previously found in unoperated duodenal ulcer patients.

Adult↗
PubMed1978

Reappraisal of the sympathetic role in the sphincteric urethra. Denervation supersensitivity of the urethra of the chronic neurogenic bladder to alpha-adrenergic drugs.

The response of urethral pressure to administration of an alpha-stimulant was compared between a group of eight patients with chronic neurogenic bladders as evidenced by positive denervation supersensitivity to parasympathomimetic bethanechol chloride and a group of ten control patients. A supersensitive response to administration of an alpha-stimulant with a rise of maximum urethral pressure, 10 mm Hg or more above the control urethral pressure, was uniformly observed in the urethra of patients with chronically denervated bladders. Our results appear to add pharmacologic evidence of alpha-adrenergic predominance over the parasympathetic in the urethra which is believed to be innervated dually in the recently envolving new concept.

Adolescent↗
PubMed1988

Cyclic GMP inhibits protein kinase C-mediated secretion in rat pancreatic acini.

Dibutyryl cyclic GMP (Bu2cGMP) inhibited agonist-induced secretion of amylase from isolated rat pancreatic acini. In contrast to previous studies, this inhibitory action was not confined to butyryl derivatives of cyclic GMP, since the membrane-permeant cyclic GMP analogues Bu2cGMP and cyclic 8-bromo-GMP (8-Br-cGMP) were equipotent (IC50 2 nM) in their inhibition of amylase secretion stimulated by cholecystokinin-(26-33)-octapeptide (CCK8): at extracellular concentrations up to 1 mM, cyclic GMP itself was devoid of inhibitory activity. Both Bu2cGMP and 8-Br-cGMP also potently inhibited secretion stimulated by 4 beta-phorbol 12-myristate 13-acetate (PMA) (IC50 6 nM), but only partially inhibited responses elicited by bethanechol or bombesin and were without effect on A23187-evoked secretion. Furthermore, agents that are known to raise intracellular cyclic GMP levels (MB22948 (2-o-propoxyphenyl-8-azapurin-6-one) or nitroprusside) or antagonize the actions of protein kinase C (4 alpha-PMA or staurosporine), also inhibited CCK8- or PMA-stimulated secretion but not secretion elicited by bombesin, bethanechol, or A23187. It is concluded from these and other observations reported here that protein kinase C is the major intracellular mediator of amylase secretion stimulated by CCK8 and that this pathway may be regulated by cyclic GMP at a step that follows protein kinase C activation.

Amylases↗
PubMed1977

In vivo cholinergic stimulation of the rabbit oviductal musculature.

The in vivo activity of the rabbit oviductal musculature was evaluated in terms of constant rate perfusion resistance. Efforts to compare adrenergic and cholinergic stimulation showed that both pilocarpine and bethanechol chloride increased muscular activity 17-24% of that induced by epinephrine. The cholinergic stimulatory effect was reduced by adrenergic alpha blockade and completely abolished by cholinergic blockade or norepinephrine depletion. The data suggest that cholinergic stimulation of the tubal musculature is mediated, in part, via postganglionic adrenergic nerve fibers. It would appear that the oviductal musculature is not a primary target tissue for systemically administered autonomic agonists or antagonists.

Animals↗
PubMed1988

Acetylcholine produces cerebrovascular constriction through activation of muscarinic-1 receptors in the newborn pig.

This study was designed to characterize the nature of responses to selective muscarinic (M)-1 and M-2 agonists and to determine the receptor subtype which mediates the vascular response to acetylcholine in the cerebral circulation of the newborn pig. Pial arterioles of anesthetized newborn pigs were observed using the closed cranial window method. Topical McN-A-343 (10(-7), 10(-4) M), an M-1 agonist, produced pial arteriolar constriction (diameters were 140 +/- 8, 127 +/- 9 and 111 +/- 8 microns for control, 10(-7) and 10(-4) M McN-A-343) that was blocked by topical pirenzepine (10(-3) M), an M-1 antagonist. Topical bethanachol (10(-7), 10(-4) M), an M-2 agonist, produced pial arteriolar dilation (diameters were 148 +/- 8, 169 +/- 10 and 181 +/- 10 microns for control, 10(-7) and 10(-4) M bethanachol) that was blocked by 4-DAMP 4-diphenylacetoxy-N'-methylpiperidine methiodide (10(-3) M), an M-2 antagonist. Responses to McN-A-343 were unchanged after 4-DAMP, and responses to bethanachol were unchanged after pirenzepine. Topical McN-A-343 and bethanachol elicited modest increases in cortical periarachnoid cerebrospinal fluid levels of 6-keto-prostaglandin F1 alpha, prostaglandin E2, thromboxane B2 and prostaglandin F2 alpha. Topical acetylcholine (10(-7), 10(-4) M) elicited pial arteriolar constriction and large increases in cerebrospinal fluid prostanoid levels which were blocked by atropine (0.5 mg/kg i.v.) and topical pirenzepine (10(-3) M), but not by topical 4-DAMP. These data demonstrate the existence of M-1 and M-2 receptors in the cerebral circulation of the newborn pig and indicate that acetylcholine elicits cerebrovascular constriction and increased cerebrospinal fluid prostanoid synthesis via activation of M-1 receptors.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Combined effect of disopyramide and bethanechol: use of bethanechol to prevent anticholinergic side effects of disopyramide without reduction of antiarrhythmic efficacy.

Because bethanechol chloride (B) relieves the anticholinergic side effects of disopyramide (D), we examined the combined effects of D and B on the heart and urinary bladder. B was confirmed to counteract dose dependently the effect of D on the dog bladder. In the ventricular muscle, the combined electrophysiological effects (D + B) were additive, with no reduction in the effect of D. With the control value set as 100%, the decrease in the maximum rate of depolarization with 5 X 10(-6) g/ml D (90 +/- 6%) was not affected by the same dose of B (D + B: 84 +/- 14%). Moreover, the effective refractory period (ERP) was larger with D + B (128 +/- 12%) than with either B (109 +/- 9%, p less than 0.01) or D (115 +/- 11%, p less than 0.05). In contrast, in the atrial muscle and AV and SA nodes, B had marked acetylcholine-like effects. These were completely suppressed by the addition of D except for the atrial ERP with the highest tested concentration of B (5 X 10(-6) g/ml). In the latter case, the prolongation of ERP was minimal (B + D: 105 +/- 14%) as compared with D alone (130 +/- 15%). Since the plasma concentration of B after oral administration of a clinical dose is expected to be on the order of 10(-7) g/ml, no practical effect is anticipated. We conclude that B can be expected to counteract urination disorders caused by D without reducing D's antiarrhythmic efficacy.

Anesthesia↗
PubMed1989

Forskolin stimulation of pepsinogen secretion from frog esophageal mucosa is partly mediated by intrinsic cholinergic neurons.

Forskolin was found to stimulate pepsinogen secretion from frog esophageal mucosa. The stimulation was dose-dependent and was accompanied with a great increase in tissue cAMP content. The response to forskolin mimicked the action of bethanechol and was not additive with bethanechol. The stimulatory effect of forskolin was inhibited by 50% in the presence of either atropine or tetrodotoxin. On the other hand, incubation in a calcium-free medium not only reduced the response to forskolin by 45% but also eliminated the influence of atropine and tetrodotoxin. These results indicate that forskolin may stimulate pepsinogen secretion from the frog esophageal mucosa via activating adenylate cyclase, and part of its effect may arise from eliciting acetylcholine release from the intrinsic neurons.

Animals↗
PubMed1989

[A case of ureteral and vesical malacoplakia].

A case of ureteral and vesical malacoplakia is reported. A 58-year-old woman was admitted for non-papillary sessile bladder tumor. Ultrasound examination revealed bilateral hydronephrosis and renal function was deteriorated. Escherichia coli and beta-streptococcus were isolated from her urine. Antegrade pyelography demonstrated obstruction of the bilateral ureters. Percutaneous pyeloscopy revealed a bean-sized yellow nodule at the upper portion of the right ureter. Pathohistological the lesions of aggregates of macrophage in which typical Michaelis-Gutmann bodies were found at the punch biopsies of both vesical and ureteral lesions. She was treated successfully with the administration of bethanechol chloride and antibiotics. This case seems to be the second report of ureteral malacoplakia in the Japanese literature.

Bethanechol↗
PubMed1989

Serotonin depletion potentiates gastric secretory and motor responses to vagal but not peripheral gastric stimulants.

Vagal stimulation is known to release gastrointestinal serotonin. The effect of depletion of serotonin stores on vagally stimulated gastric acid secretion and motility was studied in rats. Pretreatment of rats with parachlorophenylalanine (p-CPA) did not alter basal gastric acid and serotonin secretion but produced a 57% reduction in the intraluminal gastric release of serotonin and a 43 to 100% potentiation of the gastric acid secretory response elicited by intracisternal injection of the stable thyrotropin-releasing hormone analog, RX 77368, in conscious pylorus-ligated rats or urethane-anesthetized rats with an acute gastric fistula. Dose-response studies revealed that the gastric acid secretion induced by submaximal but not high doses of RX 77368 was elevated significantly by p-CPA pretreatment. p-CPA also enhanced the gastric acid output produced by submaximal, but not high doses of the vagal stimulant baclofen, [beta-(p-chlorophenyl)-gamma-aminobutyric acid]. In contrast, p-CPA pretreatment had no effect on gastric acid secretion stimulated by bethanechol, histamine or pentagastrin. Selective depletion of central serotonin stores by pretreatment with the neurotoxin 5,7-dihydroxytryptamine given alone, or combined with parachloroamphetamine did not alter RX 77368-stimulated gastric acid secretion. In addition, gastric contractility stimulated by intracisternal injection of RX 77368 was significantly enhanced by p-CPA but not by 5,7-dihydroxytryptamine pretreatment, whereas the contractile response to carbachol was not altered by p-CPA pretreatment. These results suggest that depletion of peripheral but not central serotonergic stores potentiate gastric acid secretion and contractility induced by vagally, but not peripherally acting gastric stimulants. Thus, peripheral serotonin may exert an inhibitory tone on vagally stimulated gastric acid secretion and motility in the rat.

Animals↗
PubMed1989

Quantitation by computerized visual image analysis of gastric mucosal lesions induced in mice and rats by non-steroidal anti-inflammatory drugs.

A method is described for the quantative determination of gastric mucosal lesions induced by non-steroidal anti-inflammatory drugs in mice and rats. The area and number of gastric lesions present in formalin-fixed, glycerol-cleared mucosa is determined by computerized visual image analysis using instrumentation as described. The method is also applied to the determination of the protective effects of anti-ulcer agents (e.g. prostaglandin E2, pirenzepine). Thus this method affords unambiguous sensitive and determination of the percentage area of the mucosa damaged and the number of the lesions.

Animals↗
PubMed1989

Drug therapy of reflux oesophagitis: an update.

The various therapeutic approaches for reflux oesophagitis are to enhance oesophageal clearance, to coat damaged tissue, to increase the competence of the reflux barrier, to reduce the volume and pH of gastric contents, and to improve gastric emptying and pyloric sphincter competence. Unfortunately, drug therapy of reflux oesophagitis is not yet ideal. Of the prokinetic agents, cisapride is the only drug with proven benefit. Single-agent therapy with the H2-receptor antagonists or sucralfate results in similar degrees of symptom relief and healing. Rapid symptom relief and healing are achieved by omeprazole; however, the significance of sustained achlorhydria remains to be established. Dinnertime dosing of cimetidine appears to be a rational method of suppressing late-evening gastric acidity. Patients with severe or recalcitrant disease should not be treated with conventional therapy alone; the results of controlled studies of combination therapy with the H2-receptor antagonists and sucralfate or cisapride will be viewed with interest.

Antacids↗
PubMed1989

An embryonic Ca++ mobilizing muscarinic system in the chick embryo heart.

In the embryonic and in the adult heart muscarinic stimulation reduces the heart rate. Here we demonstrate that in the embryonic heart an additional muscarinic system is present, which is characterized by Ca++ mobilization and corresponds to the embryonic muscarinic system in other organ anlagen. In suspensions of embryonic chick heart cells we measured release of Ca++ from intracellular stores and influx of extracellular Ca++ with fura-2 and chlorotetracycline after muscarinic stimulation and determined the [3H]quinuclidinylbenzilate binding sites. We observed intense Ca++ mobilization at day 4, weaker reactions between day 4.5 and 11, and no Ca++ response at day 13. The pharmacological profile was identical to the profile of Ca++ mobilization in cells from other embryonic tissues in which the general embryonic muscarinic system is expressed. In parallel, we studied the effect of muscarinic agonists and antagonists on the heart rate of isolated embryonic hearts at day 4 and 5 in a perfusion chamber. Oxotremorine and bethanechol being antagonists or weak partial agonists in Ca++ mobilization, behaved as full agonists in frequency regulation. Thus, the pharmacological profile of the transient embryonic muscarinic system was different from that of the definitive adult form.

Animals↗
PubMed1985

Effects of substance P on cholinergically stimulated gastric acid secretion and mucosal blood flow in rats.

Effects of substance P (SP) on gastric acid secretion and mucosal blood flow (MBF) were examined in anesthetized Wistar rats. Intravenous infusion of graded doses of SP (5 and 10 nmol/kg/min) had no effects on either the basal gastric acid secretion or on the MBF. When gastric acid secretion was increased by giving a supramaximal dose of bethanechol (10 micrograms/kg/min), a muscarinic parasympathetic stimulant, SP had no effect on the gastric acid secretion but did decrease the MBF. On the other hand, when gastric acid secretion was increased by left cervical vagus nerve stimulation (0.5 mA, 3 Hz, 0.5 msec duration), SP inhibited both acid secretion and MBF, in a dose-dependent manner. The inhibitory effects of SP on the vagally stimulated gastric responses were not affected by pretreatment with phentolamine (5 mg/kg i.m.), propranolol (10 mg/kg i.m.), mepyramine (20 mg/kg i.m.) or indomethacin (30 mg/kg i.v., followed by 4 mg/kg/hr). These findings suggest that SP acts directly on the gastric vascular system and decreases gastric MBF, and that this substance also acts on the parasympathetic neurons in the gastric wall and inhibits the vagally stimulated gastric acid secretion. The inhibitory effects of SP on the gastric acid secretion do not appear to be mediated by adrenergic or by histamine H-1 receptor-, prostaglandin-involved mechanisms.

Animals↗
PubMedDate not supplied

Pirenzepine prevents cysteamine-induced formation of gastroduodenal ulcers and reduction of mesenteric circulation.

The effects of pirenzepine on gastric and duodenal ulceration and barrier mucus levels, as well as on changes of superior mesenteric artery diameter caused by cysteamine, were investigated in rats and compared with those of atropine. Cysteamine induced severe gastric and duodenal ulcers and decreased both barrier mucus levels and mesenteric blood flow. Pirenzepine reduced gastric and duodenal ulceration induced by cysteamine. Moreover, pirenzepine significantly increased basal mesenteric artery diameter and fully prevented cysteamine-induced decrease in mesenteric blood flow. Under the same conditions, atropine failed to prevent gastric and duodenal ulceration or mesenteric artery changes caused by cysteamine. Both pirenzepine and atropine were without any effect on cysteamine-induced inhibition of gastric and duodenal barrier mucus levels. The present results are consistent with the view that pirenzepine protects against gastroduodenal ulceration caused by cysteamine by increasing blood flow at the level of the ulcerated mucosa. The higher affinity of pirenzepine for the muscarinic receptors of sympathetic ganglia may explain the difference between the effects of pirenzepine and atropine. In addition to this, the measurement of superior mesenteric artery diameter changes may represent an accurate and reproducible method, suitable for studying the gastrointestinal protective mechanisms of the drugs.

Animals↗
PubMed1985

Self-cancellation of drug properties as a mode of organ selectivity: the antimuscarinic effects of ambenonium.

Ambenonium is known to be an inhibitor of acetylcholinesterase, and recent data have shown this drug to antagonize muscarinic receptors as well. This latter property was confirmed by Schild analyses of ambenonium-induced blockade of responses to bethanechol in guinea-pig ileal longitudinal smooth muscle, taenia caeci, trachea and rat anococcygeus muscle. Statistical analysis showed ambenonium to be a simple competitive antagonist of responses to bethanechol in these tissues with pKB values in each tissue not significantly different from each other (mean pKB = 6.0). However, considerable variability in pKB estimates was encountered when ambenonium was utilized to block responses to acetylcholine. Ambenonium was a less potent antagonist of tissue responses to acetylcholine, and the underestimation in the pKB (as compared to that obtained with bethanechol) could be eliminated by prior treatment of tissues with the acetylcholinesterase inhibitor neostigmine. These data suggested that ambenonium had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of acetylcholinesterase and concomitant antagonism by blockade of muscarinic receptors. The Schild regressions obtained for ambenonium antagonism of acetylcholine responses formally satisfied criteria for simple competitive antagonism of a homogenous population of receptors (linear regression, slope equal to unity). The fact that these regressions yielded erroneous apparent pKB values suggests how two properties of a drug in one molecule could provide misleading information about drug receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗