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PubMed1991

[A case of malakoplakia of the kidney and urinary bladder].

A case of malakoplakia which co-existed in the kidney and the urinary bladder is reported. The patient was a 51-year-old female who had been suffering from asymptomatic macroscopic hematuria. Cystoscopic examination revealed multiple yellow-red nodules in the posterior and lateral wall of the bladder. Transurethral punch biopsy of the mucosa was performed and histopathological examination of the specimens revealed the diagnosis of malakoplakia. The laboratory data at admission were within normal limits except for slightly accelerated erythrocyte sedimentation rate. The culture of urine was negative. The cytology of urine was interpreted as Papanicolaou class I. Intravenous pyelography demonstrated filling defect of the left upper renal calyx, which was confirmed by retrograde pyelography. Computerized tomography showed dilatation of the left upper calyx. An exploratory operation disclosed that the upper calyceal neck was obstructed by several small nodular lesion, which were very similar to the lesions in the bladder. Because intraoperative pathological diagnosis of the frozen section was malakoplakia, partial nephrectomy was performed. Histopathological examination of the kidney and the bladder showed typical Michaelis-Gutmann bodies in the granulomatous lesions. Follow-up examinations 4 months after operation revealed some residual lesions in the bladder which were treated with bethanechol, but no recurrence in the kidney.

Bethanechol↗
PubMed1991

Stable bimodal response to cholinomimetic drugs in Alzheimer's disease. Brain mapping correlates.

We investigated quantitative EEG brain mapping as a physiologic marker of drug response while studying the stability of intersubject variability in patients with Alzheimer's disease (AD) who were receiving bethanechol through intracerebroventricular (ICV) shunts. Two of the patients had previously demonstrated cognitive and behavioral improvements on medication; the third had cognitive deterioration complicated by agitated depression. All three patients were reexamined in a dose-response paradigm. Serial brain mapping examinations were performed along with brief cognitive testing. All patients showed drug responses that were comparable with responses during their initial dose-response phase. There were strong linear correlations between global decreases in 2 to 6 Hz slow-wave activity and cognitive improvement. Brain mapping demonstrated that slowing decreased in magnitude and field with increasing dose until optimal dose was reached; with supra-optimal doses, the magnitude and field of the slowing increased dramatically. These results suggest that the quality of cholinomimetic drug responses are stable over time in individual patients, and that magnitude and pattern of slow-wave activity as measured by brain mapping may be useful in monitoring treatment with cholinomimetic agents.

Alzheimer Disease↗
PubMed1991

Neurotransmitter modulation of calcium channels in rat sympathetic neurons.

Adrenergic, cholinergic, and a variety of peptide neurotransmitters are known to modulate Ca currents in peripheral neurons. Using a protocol that allows for simultaneous assessment of effects on dihydropyridine (DHP)-sensitive and DHP-insensitive current components, we compared the actions of norepinephrine (NE), bethanechol (BeCh), and neuropeptide Y (NPY) on Ca currents in neonatal rat superior cervical ganglion neurons. Here, we show that these transmitters selectively depress the activity of DHP-insensitive Ca channels. Intracellular application of GTP-gamma-S, an activator of GTP-binding proteins, also exclusively affected the DHP-insensitive current, whereas 1,2-oleoylacetylglycerol (OAG), a protein kinase C (PKC) activator, depressed both the DHP-sensitive and DHP-insensitive currents. Pertussis toxin interrupted the coupling between NE and its effector, whereas three different inhibitors of PKC did not. Thus, we confirmed that the selective actions of the transmitters on Ca current appear to be mediated via GTP-binding proteins, but we found no evidence for direct involvement of PKC and conclude that the observed actions of OAG are distinct from those mediated by the neurotransmitters studied.

Animals↗
PubMed1991

A syndrome resembling feline dysautonomia (Key-Gaskell syndrome) in a dog.

Dysautonomia, or autonomic nervous system dysfunction, was diagnosed in a 1-year-old dog. Clinical signs of disease included diarrhea, vomiting, prolapse of nictitating membranes, and urinary incontinence. Bilateral keratoconjunctivitis sicca, xerostomia, and decreased anal sphincter tone were also observed. On the basis of response to atropine, results of intradermal histamine testing and gastric motility studies, and ocular response to parasympathomimetics and sympathomimetics (direct and indirect acting), autonomic nervous system function was determined to be abnormal. Treatment with metoclopramide hydrochloride and bethanechol chloride resulted in improved attitude, appetite, Schirmer tear test response, and decrease in frequency of vomiting within 24 hours. Bladder function and anal tone improved within 3 weeks.

Animals↗
PubMed1975

Effects of drugs influencing gastric secretion on the quantitative histological distribution of cyclic adenosine 3':5'-monophosphate in the rat stomach.

To help clarify conflicting evidence on the cyclic adenosine 3':5'-monophosphate (cyclic AMP) role in acid secretion in the rat stomach, and to establish the quantitative effects on cyclic AMP concentrations in histological regions of the glandular stomach of the 24-hr fasted rat of injections of drugs that stimulate or inhibit gastric secretion, the concentrations were measured by the firefly luminescence method using fresh-frozen microtome tissue sections cut serially through the stomach wall. The data are compatible with cyclic AMP involvement in the acid secretion. Parietal-mucous neck cell cyclic AMP levels (3.3,0.11 means, expressed as picomoles per mg of wet weight and picomoles per mug of protein-nitrogen, respectively) were the highest in any region. Pentagastrin or urecholine elevated these values slightly, and theophylline produced greater increases in all regions (parietal-mucous neck cell, 5.4, 0.22), but theophylline administered either with pentagastrin or urecholine further elevated the values (8.3, 0.31). Urecholine or pentagastrin plus theophylline each generated two approximately equal cyclic AMP concentration peaks (about one-half parietalmucous neck cell concentrations (2.7, 0.22), perhaps by negative feedback, but low dose (2 mg per kg) elevated these values more than pentagastrin or urecholine, and with theophylline they were greatly increased (9.1, 0.32). The inhibitors, atropine and prostaglandin E2, alone or with theophylline, had little influence on parietal-mucous neck cell cyclic AMP levels but caused an increase in chief cell and muscle zones.

Animals↗
PubMed1991

Bethanechol and phenylephrine responses in canine inferior vena cava and abdominal aorta.

Both canine inferior vena cava and abdominal aorta showed a concentration dependent increase of contraction in response to phenylephrine; however, inferior vena cava contracted in response to bethanechol but abdominal aorta did not respond to bethanechol. When the inferior vena cava was preconstricted with 1 x 10(-3)M bethanechol, low concentrations of phenylephrine (1 x 10(-7)M to 1 x 10(-6)M) induced relaxation, but relaxation by phenylephrine of abdominal aorta pretreated with 1 x 10(-3)M bethanechol did not occur.

Animals↗
PubMed1991

Effects of locus coeruleus activation on electroencephalographic activity in neocortex and hippocampus.

Experiments were conducted to examine the hypothesis that increased neuronal discharge activity of noradrenergic neurons of the locus coeruleus (LC) above resting discharge rates can alter forebrain electroencephalographic (EEG) activity. Small infusions (70-135 nl) of the cholinergic agonist bethanechol within 500 microns of the LC were used to activate this nucleus reversibly in halothane-anesthetized rats. A combined recording-infusion probe allowed verification of this electrophysiological activation. Simultaneously, EEG activity was recorded from sites in the frontal cortex and hippocampus and subjected to power-spectrum analyses. The findings were (1) LC activation was consistently followed, within 5 to 30 sec, by a shift from low-frequency, high-amplitude to high-frequency, low-amplitude EEG activity in frontal neocortex and by the appearance of intense theta-rhythm in the hippocampus; (2) forebrain EEG changes followed LC activation with similar latencies whether infusions were made lateral or medial to the LC; (3) infusions placed outside the immediate vicinity of the LC were not followed by these forebrain EEG effects; (4) following infusion-induced activation, forebrain EEG returned to preinfusion patterns with about the same time course as the recovery of LC activity (10-20 min for complete recovery). These infusion-induced effects on EEG activity were blocked or severely attenuated by pretreatment with the alpha 2-agonist clonidine, which inhibits LC discharge and norepinephrine release, or the beta-antagonist propranolol. These observations indicate that enhanced LC discharge activity is the crucial mediating event for the infusion-induced changes in forebrain EEG activity observed under these conditions and suggest that LC activation may be sufficient to induce EEG signs of cortical and hippocampal activation.

Animals↗
PubMed1991

Existence of ATP-evoked ATP release system in smooth muscles.

Effects of stable ATP analogs such as alpha,beta-methylene ATP (alpha,beta-mATP) and beta,gamma-methylene ATP (beta,gamma-mATP) on ATP release and contractile response were evaluated in the vas deferens and ileal longitudinal muscles of guinea pig. In these smooth muscles, administration of alpha,beta-mATP (10, 30 or 100 microM) produced an ATP release accompanied by a transient contraction, but alpha,beta-methylene ADP (30 or 100 microM) or adenosine (30 microM) failed to elicit both the ATP release and the contraction. However, the peak responses of ATP release and contraction to alpha,beta-mATP (100 microM) in the vas deferens appeared around 2 min and 2.62 sec, respectively, after the injection of the drug. Beta,gamma-mATP (10 or 100 microM) caused an ATP release from the vas deferens. The ATP release as well as the contraction evoked by alpha,beta-mATP or beta,gamma-mATP were effectively inhibited by 300 microM suramin, a P2 purinoceptor antagonist. By contrast, ATP release and contractile response to norepinephrine in the vas deferens and those to bethanechol in the ileum were virtually unaffected by this antagonist. Veratridine and ouabain at (30 or 100 microM) caused markedly acetylcholine release from the ileum and norepinephrine release from the vas deferens, respectively. However, alpha,beta-mATP, even in a high concentration of 100 microM, did not elicit any release of acetylcholine or norepinephrine. These findings suggest that alpha,beta-mATP and probably beta,gamma-mATP evoke ATP release from not neuronal but mainly smooth muscular sites by activating suramin-sensitive P2x receptors, implying that "ATP-evoked ATP release system" exists.

Acetylcholine↗
PubMed1991

Motor response to electric spatial stimulation of isolated intact and inflamed human appendix.

The smooth muscle responses to electric stimulation of intact, slightly or severely inflamed, isolated human appendix strips were studied. No changes were noted in the motility of the not inflamed and slightly inflamed appendices, (simple appendicitis), the preparations responded to nervous stimulation with contractions of the same size. The smooth muscle contractions were blocked by atropine, and enhanced by physostigmine, which proves the cholinergic nature of the innervation. The severe inflammation (acute phlegmonous appendicitis) reduced also the contraction and relaxation of the appendix strips. With the advancement of the inflammatory process, the decreased motility of the appendix can play an in vivo role in the rapid progress of the process.

Appendicitis↗
PubMed1991

Interactions of agonists with M2 and M4 muscarinic receptor subtypes mediating cyclic AMP inhibition.

In this study the similarities and differences between the M2 and M4 subtypes in their recognition of agonists were explored. A CHO-K1 cell line transfected with the human m2 receptor was used as a homogeneous M2 tissue for comparison with two putative M4 systems (rat striatum and the N1E-115 mouse neuroblastoma cell line). The equilibrium binding dissociation constants and intrinsic efficacies for seven muscarinic agonists were determined for their stimulation of cyclic AMP inhibition via the M2 and M4 receptors. Partial receptor occlusion with propylbenzilylcholine mustard was used to determine binding constants for the more efficacious drugs and the reference agonist oxotremorine-M. The binding dissociation constants and relative efficacies for other agonists were then determined in reference to oxotremorine-M by a null method. For the M2 receptor the agonist binding dissociation constants ranged in potency from oxotremorine (1.5 microM) to bethanechol (171 microM), whereas relative efficacies varied from that of muscarine (relative efficacy = 0.9) to the value for McN-A343 (relative efficacy = 0.04). In general, most agonists bound with similar potencies to M2 and M4 receptors (Kd values within a factor of 2-3). However, oxotremorine bound to the N1E-115 and striatal M4 receptors about 3-fold and 10-fold less potently, respectively, than it did to the M2 receptor. Another exception was pilocarpine, which bound to the N1E-115 receptor (1.9 microM) with 8-fold and 12-fold higher potency than to the CHO-K1 M2 receptor and the striatal M4 receptor, respectively. Despite the low affinity of bethanechol for the M2 receptor, it was an efficacious agonist (maximal response equivalent to that of oxotremorine-M; relative efficacy = 0.6) at this subtype, whereas it was a partial agonist (60%) with lesser efficacy in the clonal M4 system. In contrast, McN-A343 and arecoline were significantly more efficacious at the two M4 receptors than they were at the M2 receptor. The M4 system in the rat striatum displayed some similarity to the N1E-115 M4 system, with regard to the efficacy ranking for certain agonists (arecoline greater than bethanechol greater than McN-A343 greater than or equal to pilocarpine). This rank order was different from the ranking of these four agonists in the M2 system, indicating that these two M4 receptors are more similar to each other in efficacy ranking than they are to the M2 receptor. However, the rat striatal and N1E-115 M4 receptor differed in their binding of oxotremorine and pilocarpine, indicating that these two M4 systems were not pharmacologically identical.(ABSTRACT TRUNCATED AT 400 WORDS)

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1991

Muscarinic inhibition of pancreatic B-cells.

Muscarinic agonists are known to potentiate insulin secretion and increase glucose-induced firing of pancreatic B-cells. Here we report two experimental situations in which inhibitory effects of muscarinic agonists may be observed. (1) Muscarinic agonists delay the onset of the 11.1 mM glucose-induced cell depolarization. (2) At concentrations between 10(-9) and 10(-7) M, acetyl-beta-methylcholine (and also bethanechol and MCN-a-343) decreases cell input resistance and decreases insulin release of islet cells exposed to 5.6 mM glucose.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1991

Evidence of a direct TRH effect on the rat exocrine pancreas.

In the present study, the effect of TRH on amylase secretion was determined both in vivo, by cannulating the pancreatic duct of rats, as well as in vitro, by using isolated lobules and dissociated acini. The results show that TRH inhibited both basal and stimulated in vivo amylase secretion. Nevertheless, the in vitro experiments failed to show a TRH-related inhibitory effect when TRH was used alone, although the hormone did blunt the secretion elicited by CCK8 and bethanechol from isolated lobules and dissociated acini. Results suggest that TRH can inhibit stimulated amylase secretion in rats through a direct effect on acinar cells.

Amylases↗
PubMed1991

Gastric juice and analysis of basal and stimulated secretion following treatment with rice-bran oil.

In determining whether rice-bran oil (RBO) has antisecretory activity, we induced stress ulcers in 20 Wistar rats (10 controls; 10 animals given 0.2 ml/day RBO orally for 4 days prior to ulcer induction). In turn, we analyzed gastric juice for histamine, pepsin, H+ concentration ([H+]) and output volume. A second, complementary study was made of basal and stimulated gastric secretion through continuous "in vivo" recording of output. Secretion was stimulated with increasing doses of histamine, betanechol and pentagastrin. Ninety-four rats were used (47 controls and 47 rats given 0.2 ml/day RBO orally for 4 days prior to gastric output evaluation). The results were evaluated by the Student t-test. Ulcer index in the RBO-treated rats was significantly lower than among the controls (p less than 0.01), as also reflected by a significantly greater decrease in [H+] among the RBO-treated rats (p less than 0.05). However, no significant differences were observed for the remaining parameters. Continuous recording of basal gastric output showed a significant decrease in [H+] among the RBO-treated rats (p less than 0.01). Following histamine stimulation, [H+] was likewise significantly lower among the RBO-treated rats than in the controls. However, no significant differences were observed following stimulation with either betanechol or pentagastrin. RBO contains a high percentage of unsaturated fats; the latter act as precursors in the synthesis of arachidonic acid, which in turn is the essential precursor of prostaglandins--established inhibitors of gastric secretion. RBO also contains antioxidants such as alpha-tocopherol, which may likewise stimulate the synthesis of prostaglandins. RBO likely acts by increasing prostaglandin output, thus interfering with gastric HCl production.

Administration, Oral↗
PubMed1991

Role of cholecystokinin in postprandial and vagally stimulated duodenal and gallbladder motility in dogs.

This study was designed to determine the role of cholecystokinin (CCK) in postprandial motility pattern of the duodenum and gallbladder (GB) in conscious dogs provided with chronic duodenal electrodes for recording of myoelectric activity and GB fistulas for measurement of intraluminal pressure and volume of GB and to calculate the GB motility index (MI) and GB emptying rate. During naturally occurring activity front (phase III MMC) in the duodenum there was significant increase in the MI of GB accompanied by about 20-30% reduction in the GB volume. These changes in duodenal and GB motility pattern could be duplicated by i.v. motilin. Feeding abolished the appearance of spontaneous activity front in the duodenum and greatly increased motility of GB while reducing its volume. Administration of CCK receptor antagonists in fed dogs failed to affect the motility changes induced by meal in the duodenum but abolished these of the GB. Vagal cholinergic stimulation with insulin, 2DG or urecholine caused similar effects to that induced by food i.e. increased duodenal spike activity, abolished phase III of the MMC, decreased GB volume and increased GB motility. Pretreatment with CCK antagonists did not affect significantly duodenal spike activity or GB motility but significantly increased the GB volume. Atropine 125 micrograms/kg) blocked almost completely spontaneous activity front in the duodenum and accompanying alterations in the motility and volume of GB. We conclude that CCK contributes to the MMC related alterations in the GB motor activity and is essential in cholinergic stimulation induced of the GB emptying but not in vagally induced duodenal and GB motility.

Animals↗
PubMed1990

Pharmacologic characterization of the changes in cholinergic sensitivity of rat jejunal circular muscle after myenteric plexus ablation.

Neurons located in the myenteric plexus are generally believed responsible for motor control of intestinal circular muscle. The in vitro isometric responses of naive and myenterically denervated (MD) rat jejunal circular muscle to bethanechol and carbachol, alone and in the presence and absence of neuronal antagonists (hexamethonium bromide, tetrodotoxin and Botulinum toxin A) 15 and 30 days after myenteric plexus ablation, were determined. The responses to bethanechol indicated no differences in muscarinic sensitivity between naive and MD tissue. The relative potency of carbachol, which acts at both muscarinic and nicotinic receptors, in MD tissue 15 days after denervation was significantly higher than that in naive tissue. However, 30 days after denervation, the relative potencies of carbachol in naive and MD circular muscle were comparable. The presence of neuronal antagonists had no effect on the relative potency of carbachol 15 days after myenteric denervation, but altered significantly the responses 30 days after denervation. The effects produced by the neuronal antagonists 30 days after myenteric denervation were qualitatively and quantitatively different than those produced in naive tissue, suggesting that the nature of the innervation in these tissues was different. These results demonstrate that circular muscle was denervated initially after myenteric plexus ablation but reinnervation occurred within 30 days. The reinnervation observed is likely due to neurons located in the submucosal plexus.

Animals↗
PubMed1990

Cholinoceptive pontine reticular structures modify the postural adjustments during the limb movements induced by cortical stimulation.

1. Activation of the pontine reticular formation (pRF) and the related medullary inhibitory reticulospinal (RS) system decreases the postural activity. This effect can be achieved either by local injection into the dorsal pontine tegmentum of cholinergic agonists which excite cholinoceptive pRF neurons, or by injection of noradrenergic agents which block the inhibitory influence exerted by the locus coeruleus (LC) neurons on the pRF. The main aim on the present study was to analyze the effects of tonic activation of these pRF neurons on the postural adjustments accompanying limb movements induced by motor cortex stimulation. In particular, electrodes were implanted chronically in the motor cortex of cats and stainless steel guide tubes of small size, later used for drug injection, were set bilaterally into sites just above the responsive regions. 2. Limb flexion elicited by stimulation of the motor cortex was accompanied by a diagonal pattern of postural adjustment, characterized by a decreased force exerted by the limb diagonally opposite to the moving one and an increased force exerted by the other two. 3. Microinjection into the pRF of both sides of 0.25 microliter of the muscarinic agonist bethanechol at the concentration of 8 or 16 micrograms/microliters in buffered artificial cerebrospinal fluid produced a short-lasting episode of postural atonia followed by a period of reduced postural activity, during which the cats were still able to stand on the measurement platform. Under this condition no changes in threshold, latency and amplitude of the flexion response were observed in the performing limb; however, the postural responses were considerably affected. In particular, when the performing limb was a forelimb, the other anterior limb showed a dissociation of the postural response in two distinct components. The first anticipatory component, which had a short latency (12-15 msec) and was considered to be centrally triggered, decreased in amplitude after injection of bethanechol and sometimes disappeared; on the other hand the second component, which had a long latency (50-60 msec) and was thus considered to be of reflex origin, increased in amplitude, due to the instability resulting from the depression of the early postural response. Similar results also affected to a lesser extent the hindlimbs. Moreover, body oscillations were observed and monitored from the force platforms following the late component of the postural responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Bethanechol↗
PubMed1990

Intraesophageal balloon distention versus drug provocation in the evaluation of noncardiac chest pain.

Intraesophageal balloon distention (IEBD) has been advocated as an effective provocative test for the evaluation of chest pain and dysphagia. The normal esophageal response to intraesophageal balloon distention is to generate a sustained contraction proximal to the balloon while showing a distinctive absence of activity distal to the balloon. We evaluated intraesophageal balloon distention in 62 patients with noncardiac chest pain and compared the diagnostic results to those obtained by using a combination of acid infusion, edrophonium (80 micrograms/kg iv) and bethanechol (80 micrograms/kg sq). These 62 patients were also compared with 10 normal volunteers who underwent intraesophageal balloon distention. Abnormal distal manometric activity consistent with spasm and was seen in 38/62 (61%) patients. Distal manometric activity was not seen in any normal volunteer. Diagnostic results (symptom reproduction with manometric changes but without EKG changes) were seen in 26/62 (42%) patients, but in nine of the 62 (14%) patients with combined drug provocation (p less than 0.05). Intraesophageal balloon distention is superior to a combination of provocative drugs in evaluating noncardiac chest pain symptoms. The presence of abnormal manometric activity distal to the balloon may represent regulation of esophageal motility.

Bethanechol↗