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At least 955 records · Page 53Linked to original sources
PubMed1992

Differential inhibition of cholinergic and noncholinergic neurogenic contractions by 5-hydroxytryptamine1A receptor agonists in guinea pig ileum.

Previous studies have shown that 5-hydroxytryptamine1A (5-HT1A) receptors are localized only to a subset of myenteric neurons in guinea pig ileum; the purpose of this study was to determine the possible functional significance of this differential receptor localization. Nerve-mediated contractions of the longitudinal muscle, myenteric plexus of guinea pig ileum were studied in vitro. Contractions were evoked by single transmural electrical stimuli (0.5-msec duration, at 0.1 Hz; cholinergic) or trains of stimuli (10 or 20 Hz for 1 sec; noncholinergic; scopolamine, 1 microM present). The 5-HT1A agonist, 8-hydroxy-2-(n-dipropylamino)tetralin (DPAT), reduced cholinergic contractions by no more than 14% in the concentration range of 0.001 to 0.3 microM. At high concentrations (1 to 100 microM), DPAT inhibited longitudinal muscle, myenteric plexus contractions; the EC50 was 6 microM. 5-Hydroxytryptamine (5-HT) and 5-carboxamidotryptamine (5-CT) reduced longitudinal muscle, myenteric plexus contractions by a maximum of 35% and 24% at 100 and 30 microM, respectively. Spiperone and 1-(2-methoxyphenyl)-4-[4-(2-phthalimidobutyl]piperazine (NAN-190), two 5-HT1A receptor antagonists, did not block DPAT-induced inhibition of cholinergic contractions. DPAT (3, 10 and 30 microM) shifted histamine concentration-response curves to the right in an apparently competitive manner; Schild analysis yielded a pA2 of 5.2. DPAT (3, 10, 30 and 100 microM) also shifted bethanechol concentration-response curves to the right in an apparently competitive manner; Schild analysis yielded a pA2 of 5.5. These data indicate that DPAT blocks histamine and muscarinic receptors on longitudinal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Chronic ethanol feeding produces a muscarinic receptor upregulation, but not a muscarinic supersensitivity in lower esophageal sphincter muscle.

Muscarinic acetylcholine receptors (mAChR) are important in esophageal physiology, and mAChR alterations may be involved in ethanol-induced esophageal dysfunction. We previously demonstrated that acute ethanol decreases lower esophageal sphincter pressure (LESP), whereas withdrawal from chronic ethanol results in pressure increases which are reversible by acute ethanol. To see if this increase in LESP is due to upregulation of mAChR, we evaluated both mAChR binding and dose-response curves for bethanechol and atropine-induced changes in LESP before and after acute and chronic ethanol exposure. The number of mAChR sites (Bmax) in LES (3.4 fmol/mg tissue) was lowered by acute ethanol (1.72, -50%); withdrawal from chronic ethanol raised Bmax (5.2, +54%). Acute injection of ethanol into cats in withdrawal reversed this increase in mAChR density (3.1, -10%). These changes correlated with our earlier data on ethanol-induced changes in LESP. However, the dose-response curve for bethanechol-induced pressure increases shifted to the right [ED25 (micrograms/kg); control, 8.6; withdrawal, 21.3], paralleled by an increase in the number of low-affinity agonist binding sites. Thus, 1) the withdrawal-associated increase in Bmax (up-regulation) is more likely to be a compensatory response to deficits (functional subsensitivity) distal to the receptor recognition site than to proximal deficits; 2) the increase in Bmax does not cause LESP hyperactivity; and 3) receptor binding changes do not necessarily translate into physiological changes.

Animals↗
PubMed1992

Norepinephrine-induced contractile responses in isolated rat aortae from different duration of diabetes.

The present study examined contractile responses to norepinephrine in isolated aortae from 4-, 8-, and 12-week duration of streptozocin-induced diabetic rats. The pD2 value and the maximum contractile responses were significantly increased in 8-week and 12-week diabetic aortae, respectively, compared to the age-matched control aortae. Moreover, the bethanechol-induced relaxation of 12-week diabetic aortae preconstricted with norepinephrine was also significantly different from the age-matched control aortae. On the other hand, the KCl-, phenylephrine-induced contraction in 4-, 8-, and 12-week diabetic and age-matched control aortae were similar. Presumably the duration of diabetes altered the sensitivity and responsiveness of aortae to norepinephrine. The possibility of the enhanced norepinephrine response in diabetic aortae was discussed.

Animals↗
PubMed1992

Evidence for postjunctional release of ATP evoked by stimulation of muscarinic receptors in ileal longitudinal muscles of guinea pig.

The origin of the ATP release evoked by muscarinic agonists and veratridine from longitudinal muscles of the guinea pig was assessed with muscarinic antagonists. Acetylcholine (ACh) (1 microM) and bethanechol (10 microM) produced an immediate and marked ATP release, which was almost completely blocked by atropine (0.3 microM) and by the M3 muscarinic antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (1 microM); release was only slightly affected by tetrodotoxin (0.6 microM). The bethanechol-evoked release of ATP was partly, but not significantly, inhibited by pirenzepine, a M1 muscarinic antagonist. Veratridine, an ACh releaser, also elicited a delayed ATP release, in a concentration-related manner. This ATP release was greatly antagonized by atropine and by Ca++ removal from the medium, implying mediation by endogenous ACh released after depolarization. In contrast, electrically evoked ACh release was enhanced by atropine and 4-DAMP. Bethanechol, unlike veratridine, failed to elicit measurable ACh release from the tissue. The contraction evoked by bethanechol was notably inhibited by atropine and 4-DAMP, but not by pirenzepine and AFDX-116, a M2 muscarinic antagonist, at a concentration of 0.3 microM. These findings suggest strongly that ATP is postjunctionally released from the ileal smooth muscles after stimulation of postsynaptic muscarinic receptors, presumably M3 receptors.

Acetylcholine↗
PubMed1992

Muscarinic receptors in the cerebellar vermis modulate the gain of the vestibulospinal reflexes in decerebrate cats.

1. The Purkinje (P)-cells of the cerebellar vermis, which exert a prominent influence on posture as well as on the gain of vestibulospinal (VS) reflexes, are under the control not only of the classic mossy fibers and climbing fibers which liberate excitatory amino acids as neurotransmitter, but also of cholinergic afferents. The role of these afferents was investigated in precollicular decerebrate cats by using the method of local microinjection of cholinergic agents into appropriate areas of the cerebellar cortex. 2. Unilateral injection into the vermal cortex of the culmen of the non-selective cholinergic agonist carbachol (0.25 microliters at 0.5 micrograms/microliters saline) produced a postural asymmetry, characterized by a slight decrease of the extensor tonus in the ipsilateral forelimb and an increased tonus in the contralateral forelimb. Moreover, the gain of the EMG responses of the ipsilateral and the contralateral triceps brachii to animal tilt increased significantly, while no significant changes in the phase angle of the responses were observed. These effects started 5-10 min after the injection and persisted for at least 2 hours before disappearing. Similar but smaller effects were obtained after injection of eserine, an inhibitor of acetylcholinesterase. Thus, the effects could be produced by increasing the naturally present amount of acetylcholine (ACh). 3. The changes in posture and gain of the VS reflexes described above utilized in part at least muscarinic receptors, since effects similar to those induced by carbachol injection were also obtained after unilateral microinjection into the vermal cortex of the culmen of the muscarinic agonist bethanechol (0.25 microliters at 0.1 micrograms/microliters). On the other hand opposite effects, characterized by an increased postural activity in the ipsilateral forelimb associated with a decreased activity in the contralateral forelimb, as well as by a reduced gain of the EMG responses of the triceps brachii of both sides to animal tilt were observed in other experiments after local microinjection of the muscarinic antagonist scopolamine (0.25 microliter at 4-8 micrograms/microliters saline). Evidence for muscarinic supersensitivity was obtained following repetitive injections of scopolamine into the cerebellar vermis. 4. The area which upon injection of the cholinergic agents modified the postural activity as well as the gain of the VS reflexes was located within the third and/or the fourth folium rostral to the fissura prima (culmen), at the laterality of 1.4-1.8 mm with respect to the midline.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1992

[Effects of epithelium removal and cooling on tracheal contraction in guinea pigs].

We investigated the effects of epithelium removal and cooling (32 degrees C, 27 degrees C, 22 degrees C) on isolated tracheal smooth muscle contraction induced by bethanechol (BCh), acetylcholine (ACh), histamine (Hist), and KCl in guinea pigs. The pD2 values (-logED50) increased in the epithelium damaged group compared with the intact group when ACh was administered at 37 degrees C, 32 degrees C, 27 degrees C and 22 degrees C, with histamine at all four temperature conditions, and with KCl at 37 degrees C, 32 degrees C and 27 degrees C. In both groups, the pD2 values for BCh, ACh, and KCl tended to decrease as temperature was lowered, and significant decrease in pD2 was observed at 27 degrees C. In contrast, the pD2 value for histamine tended to increase as temperature was lowered in every group. Concerning these agents, we conclude that epithelium removal and cooling exert neither significant nor consistent effect on tracheal epithelial function.

Acetylcholine↗
PubMed1977

Heartburn.

Explore the source record for details and available documents.

Antacids↗
PubMed2003

Role of leptin in the control of postprandial pancreatic enzyme secretion.

Leptin released by adipocytes has been implicated in the control of food intake but recent detection of specific leptin receptors in the pancreas suggests that this peptide may also play some role in the modulation of pancreatic function. This study was undertaken to examine the effect of exogenous leptin on pancreatic enzyme secretion in vitro using isolated pancreatic acini, or in vivo in conscious rats with chronic pancreatic fistulae. Leptin plasma level was measured by radioimmunoassay following leptin administration to the animals. Intraperitoneal (i.p.) administration of leptin (0.1, 1, 5, 10, 20 or 50 microg/kg), failed to affect significantly basal secretion of pancreatic protein, but markedly reduced that stimulated by feeding. The strongest inhibition has been observed at dose of 10 microg/kg of leptin. Under basal conditions plasma leptin level averaged about 0.15 +/- 0.04 ng/ml and was increased by feeding up to 1.8 +/- 0.4 ng/ml. Administration of leptin dose-dependently augmented this plasma leptin level, reaching about 0.65 +/- 0.04 ng/ml at dose of 10 microg/kg of leptin. This dose of leptin completely abolished increase of pancreatic protein output produced by ordinary feeding, sham feeding or by diversion of pancreatic juice to the exterior. Leptin (10(-10)-10(-7) M) also dose-dependently attenuated caerulein-induced amylase release from isolated pancreatic acini, whereas basal enzyme secretion was unaffected. We conclude that leptin could take a part in the inhibition of postprandial pancreatic secretion and this effect could be related, at least in part, to the direct action of this peptide on pancreatic acini.

Animals↗
PubMed2005

[Malacoplakia in the ureter and bladder].

We report a case of malacoplakia in the ureter and bladder. A 78-year-old woman was admitted to our department for detailed examination of hydronephrosis. A small-fingertip-sized tumorous yellowish white lesion was detected by cytoscopy at a site that appeared to be the right side of the ureteral orifice. Transurethral resection was performed on the same site. Flat yellowish white protruding lesions were seen at two sites on the right ureter. Michaelis-Gutmann bodies were observed in biopsy specimens from both the bladder and ureter, and a diagnosis of malacoplakia was made. Ascorbic acid and bethanechol chloride were administered postoperatively. Endoscopy performed three months after the operation showed that the protruding lesions in the bladder and ureter had disappeared. Narrowing of the ureter or vesicoureteral reflux has not been seen to date.

Aged↗
PubMed1975

Muscarinic cholinergic regulation of cyclic guanosine 3,5-monophosphate in autonomic ganglia: possible role in synaptic transmission.

The effects of acetylcholine, and of agents which selectively mimic or block its nicotinic and muscarinic actions, have been studied on the levels of guanosine 3,5-monophosphate (cyclic GMP) and adenosine 3,5-monophosphate (cyclic AMP) in slices of bovine superior cervical ganglion. Low doses of either acetylcholine or the muscarinic agonist, bethanechol, caused a substantial increase in the level of cyclic GMP, and slightly increased the level of cyclic AMP; the acetylcholine- and the bethanechol-induced increases in cyclic GMP were blocked by atropine, the muscarinic antagonist, but not by hexamethonium, the nicotinic antagonist. The nicotinic agonist N,N-dimethylphenylpiperazinium did not alter the level of either of the cyclic nucleotides. Dopamine increased the level of cyclic AMP and acetylcholine partially prevented this dopamine-induced increase in cyclic AMP. The data are consistent with a model for the ganglion in which muscarinic cholinergic synaptic transmission is mediated by an increase in the level of cyclic GMP in the postganglionic neurons and dopaminergic transmission by an increase in the level of cyclic AMP in these neurons.

Acetylcholine↗
PubMed1991

[Clinical evaluation in 69 cases with neurogenic bladder].

Clinical evaluation was made in 69 cases of neurogenic bladder experienced during the past 3 years. Thirty seven of the patients were male and 32 female, and they ranged in age from 4 to 88 years with an average of 63.2 years, The basic diseases of neurogenic bladder were brain lesions in 27 cases, spinal cord lesions in 18 cases, and peripheral nerve lesions in 13 cases. Three cases were of the mixed type and the basic disease was unknown in 8 cases. Cerebrovascular diseases were the most frequent, followed by spinal cord injuries and intrapelvic operations. Duration from the onset of urological symptoms to the first visit to our clinic was less than 1 month in half of the patients. The chief complaints at the first visit were pollakisuria in 25 cases (25.8%), incontinence in 18 cases (18.6%), urinary difficulty in 25 cases (25.8%) and urinary retention in 13 cases (13.4%). Urological conditions at the first visit were spontaneous urination in 53 cases (76.8%), indwelling catheterization in 12 cases (17.4%) and clean intermittent catheterization in 4 cases (5.8%). Urological complications seen at the first examination were urinary tract infections (UTI) in 27 cases (39.1%) and chronic renal failure in 2 cases (2.9%). The patients were classified by cystometrography into 3 patterns: 42 cases (60.9%) with underactive detrusor, 21 cases (30.4%) with overactive detrusor and 6 cases (8.7%) with normal detrusor. Detrusor sphincter dyssynergia was observed in 29 cases (42.0%), 40.7% had brain lesions, 44.4% spinal cord lesions, and 46.2% peripheral nerve lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗