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At least 379 records · Page 21Linked to original sources
PubMed1990

Antiulcer activity of the calcium antagonist propyl-methylenedioxyindene--II. Effects on acid secretion and gastric emptying in rats.

1. Propyl-methylenedioxyindene (pr-MDI) is an intracellularly acting calcium antagonist which protects against cold/restraint-induced stress ulcers in rats. The doses of pr-MDI which produce antiulcer activity (10-30 mg/kg i.p.) are significantly lower than those which exhibit cardiovascular effects. 2. Two potential mechanisms for the antiulcer action of pr-MDI were investigated in this study: the effects on hydrochloric acid secretion and on gastric motility (gastric emptying). 3. Bethanechol-induced hydrochloric acid secretion in acutely pylorus-ligated rats was significantly obtunded by pr-MDI (30 mg/kg i.p.), but the effect was significantly weaker than that produced by verapamil (16 mg/kg i.p.) or cimetidine (10 mg/kg i.p.). Since 30 mg/kg pr-MDI produces greater antiulcer activity than the very high dose of 16 mg/kg verapamil, it is unlikely that inhibition of acid secretion plays more than a contributory role in the antiulcer mechanism of action of pr-MDI. 4. pr-MDI (10-30 mg/kg i.p.) produced a dose-dependent slowing of gastric emptying in rats fed a methylcellulose/Phenol Red test meal, and this effect correlated well with the antiulcer action. Verapamil (16 mg/kg i.p.) did not affect gastric emptying. 5. The results indicate that a reduction of gastric motility plays a major role in the mechanism of the antiulcer action of pr-MDI.

Animals↗
PubMed1990

The influence of intravesical volume upon contractile responses of the whole bladder preparation from streptozotocin-diabetic rats.

1. The in vivo whole bladder preparation was used to correlate bladder volume with the ability of urinary bladders from control, sucrose-drinking, and diabetic rats to develop pressure in response to bethanechol or nerve stimulation. 2. Both streptozotocin-induced diabetes mellitus and sucrose-diuresis caused an increase in rat urinary bladder capacity and mass. 3. There were significant decreases in the ability of bladders from control rats to develop pressure in response to bethanechol at 1.0 ml intravesical volume, but no change in responsiveness of bladders from sucrose-drinking or diabetic rats at different intravesical volumes. Bladders from sucrose-drinking and diabetic rats developed significantly less pressure in response to bethanechol stimulation at low intravesical volumes than did bladders from control rats. 4. Bladders from diabetic rats developed significantly less pressure in response to 32 Hz stimulation at 0.2 ml intravesical volume compared to larger volumes, however, there were no differences in the responses of bladders from sucrose-drinking or control rats at any intravesical volume. 5. Bladders from control and sucrose-drinking rats had a reduced ability to empty in response to bethanechol and field stimulation at large intravesical volumes. 6. Bladders from 8-week streptozotocin-diabetic rats are able to contract and empty efficiently in response to nerve stimulation and bethanechol over a wide range of intravesical volumes.

Animals↗
PubMed1993

Role of calcium in mediating the biphasic contraction of the rabbit urinary bladder.

1. The response of the urinary bladder to field stimulation is biphasic in nature consisting of an initial phasic contraction followed by a prolonged tonic phase which lasts for the duration of the stimulation. 2. The phasic response is mediated by the release of neurohumoral transmitters, primarily acetylcholine (via muscarinic receptor stimulation) and ATP (via purinergic receptor stimulation). The tonic component is mediated entirely via muscarinic receptor stimulation. 3. The present study investigates the dependence on extracellular calcium of the phasic and tonic contractile responses to field stimulation, bethanechol, and ATP. The results can be summarized as follows: 4. Field stimulation (2 and 32 Hz) and bethanechol evoke a biphasic contractile response whereas ATP evokes only a phasic response. 5. There were no significant effects of either calcium channel blockers or calcium fee EGTA medium on either spontaneous contraction or basal tension of muscle strips. 6. The calcium channel antagonists diltiazem and verapamil inhibited both the phasic and tonic responses induced by field stimulation (both 2 and 32 Hz) in a dose dependent manner. 7. For both 2 and 32 Hz stimulation, the ED50 s for the inhibition of the tonic phases of the responses to field stimulation were significantly lower than the ED50s for the inhibition of the phasic responses. 8. The tonic phase of the responses to field stimulation were inhibited to a significantly greater degree than the phasic responses by incubation in calcium-free medium containing EGTA. 9. Both the phasic and tonic components of the response to bethanechol stimulation were inhibited equally, and followed a similar time course as the tonic component of field stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Influence of strip size and location on contractile responses of rat urinary bladder body strips.

1. We investigated the influence of strip length and dorsal or ventral location of rat urinary bladder strips on contractile responsiveness. 2. No differences occurred in the contractile responses of 0.5, 1.0 and 2.0 cm strips to field stimulation, carbachol, ATP, substance P or to KCl when the data were expressed as either absolute tension or as tension per cross-sectional area. However, correction for strip mass resulted in significant decreases in the contractile responses of the 2.0-cm strips compared with the 0.5-cm strips. 3. No differences occurred in length-tension curves for ventral and dorsal bladder strips, even though the strips from the dorsal surface appeared thinner than those from the ventral surface. 4. Strips from the ventral surface exhibited more variability in response to field stimulation and were less sensitive to atropine pre-treatment than were those from the dorsal surface. They were also less sensitive to the contractile effects of carbachol than dorsal strips. Dorsal and ventral strips were equally responsive to ATP, substance P and KCl. 5. Our data indicate that the contractile responsiveness of rat urinary bladder strips is independent of strip length. Although there are some differences between the cholinergic responsiveness of strips from the ventral and dorsal surfaces of the bladder, the differences are so small that for most studies they will probably have no influence on data interpretation.

Adenosine Triphosphate↗
PubMed1989

Muscarinic excitation and inhibition of neurons in the submucous plexus of the guinea-pig caecum.

Intracellular recordings were made from neurons in the submucous plexus of the guinea-pig caecum. Muscarinic agonists (acetylcholine, bethanechol and muscarine) depolarized about 70%, and hyperpolarized about 30% of the submucous plexus neurons. Low concentrations of pirenzepine reversibly antagonized both responses. The measured dissociation constants (KD) of 10-30 nM for the depolarizations and 1-3 nM for the hyperpolarizations suggest that each response was mediated by muscarinic M1 cholinoceptors. The muscarinic depolarization and hyperpolarization were associated with a decreased and an increased conductance, respectively, and the reversal potential for the muscarinic responses varied as the potassium concentration varied, always being around the potassium equilibrium potential. In cells depolarized by muscarinic agonists these agents appeared to decrease a potassium conductance that could also be inactivated by substance P. In approximately 30% of the submucous neurons, the slow inhibitory postsynaptic potential, elicited in response to single or repetitive focal stimuli (1-10 pulses at 20-40 Hz), appeared to consist of a large component which was sensitive to the blocking action of idazoxan (100-300 nM) and a small component which was idazoxan-insensitive. The latter (muscarinic slow inhibitory postsynaptic potential) was completely abolished by pirenzepine. The concentrations of pirenzepine which caused a 50% depression ranged from 5 to 20 nM. The muscarinic slow inhibitory postsynaptic potential was increased in amplitude and duration by physostigmine (100-300 nM). The muscarinic slow inhibitory postsynaptic potential was accompanied by a decrease in membrane input resistance, and was reversed in polarity near the potassium equilibrium potential. When muscarine induced a hyperpolarization and/or focal stimulation elicited a muscarinic slow inhibitory postsynaptic potential in the presence of idazoxan (100-300 nM), the intracellular injection of guanosine 5'-O-(3-thiotriphosphate) produced a progressive membrane hyperpolarization during which the muscarinic hyperpolarizing responses were attenuated. It is concluded that the muscarine-induced reduction in potassium conductance is mediated through a muscarinic M1 receptor which has a relatively low affinity for pirenzepine. The muscarine-induced increase in potassium conductance is probably produced by the association of a guanine nucleotide-binding regulatory protein with another muscarinic M1 receptor that has a relatively high affinity for pirenzepine.

Acetylcholine↗
PubMed1986

Effect of intragastric and intraperitoneal water and saline loads on the pharmacologic induction of drinking in rats.

Water intake, induced by subcutaneous (SC) administration of angiotensin II (AII, 200 micrograms/kg), isoproterenol (25 micrograms/kg), 5-hydroxytryptophan (25 mg/kg), and bethanechol (8 mg/kg), was reduced completely to control level by administration of either an intragastric (IG) or intraperitoneal (IP) load of distilled water (3% of body weight) prior to administration of the dipsogen. A similar load of isotonic saline given by both the IG and IP routes was either ineffective or only partially effective in reducing the dipsogenic response. The similar effectiveness of IP and IG loads of water in inhibiting the responsiveness to administration of dipsogenic agents argues against a gastrointestinal mechanism as an integral part of the feedback process limiting water intake in the rat. In addition, the lack of a significant effect of similar IP and IG loads of saline suggests that stretch of either the gastrointestinal or intraperitoneal spaces is not an important factor in the inhibition observed. A possibility exists that osmotic dilution, as a result of the water load, may play a role in the feedback inhibition of the drinking responses to the dipsogenic agents used in these studies, even though the responses were mediated via the AII receptor pathway rather than the osmoreceptor pathway.

5-Hydroxytryptophan↗
PubMed1993

Muscarinic agonists have no measurable effect on cGMP formation of rat pinealocytes.

Previous studies have shown that muscarinic agonists stimulate cGMP formation in various tissues including rat brain. As in the pineal gland cGMP formation varies considerably under various experimental conditions, in the present investigation the effects of muscarinic agonists were tested. Muscarinic agonists neither stimulated pineal cGMP formation nor affected cGMP accumulation, resulting from administration of phosphodiesterase (PDE) inhibitors, norepinephrine (NE), or sodium nitroprusside (SNP). Because muscarinic agonists are known to stimulate pineal inositol phosphate (Ip) formation we suspect that muscarine-related Ip formation does not affect cGMP formation in rat pineal gland.

1-Methyl-3-isobutylxanthine↗
PubMed1985

The action of cholinomimetic and cholinolytic agents, hemicholinium-3 and alpha- and beta-bungarotoxin on the body wall muscle of the earthworm, Lumbricus terrestris.

Strips of muscle, approximately 12 segments in length, were prepared from the body wall of the earthworm, Lumbricus terrestris, from which the nerve cord and viscera had been removed. Contractions to electrical stimulation and acetylcholine agonists were recorded using an isometric transducer. A range of nicotinic and muscarinic agonists and antagonists were tested on this preparation and the results indicate that the acetylcholine receptor on this muscle cannot be classified as either nicotinic or muscarinic. Hemicholinium-3 abolished electrically induced muscle twitches at concentrations which had no effect on the acetylcholine response. Alpha-Bungarotoxin blocked the responses to both electrical stimulation and acetylcholine while beta-bungarotoxin blocked the contractions induced by electrical stimulation but potentiated the acetylcholine contraction.

Acetylcholine↗
PubMed1987

The medical therapy of reflux oesophagitis.

Besides changes in behaviour and lifestyle we nowadays have the choice of specific drugs in the treatment of reflux oesophagitis. A distinction can be made in motility modulating drugs, which stimulate oesophageal peristalsis and LOS pressure, mucosa-protecting drugs, which form a protective layer on the oesophageal mucosa, acid neutralizing (antacids) and acid suppressing drugs (H2-receptor antagonists, omeprazole). So far the results of medical therapy of reflux oesophagitis are still suboptimal. Giving the H2-receptor antagonists with the evening meal would possibly be more appropriate. A valid alternative is the mucosa-protecting agent sucralfate. Monotherapy will probably be insufficient for full healing, which explains why trials of combination therapy (H2-receptor antagonists plus sucralfate or plus cisapride) are being conducted. If omeprazole becomes available, it will revolutionize the therapy of severe reflux oesophagitis. Many questions (dose, duration, maintenance, safety monitoring etc.) remain to be determined.

Antacids↗
PubMed1985

Effect of cholinergic agonists on muscle from rodent proximal and distal small intestine.

Proximal and distal rat small intestine was cut into strips measuring 6.0 X 10.0 mm. Strips cut along the oral-caudal axis were called longitudinal strips, whereas those cut 90 degrees to that axis were called circular strips. Stress in circular and longitudinal muscle strips was measured continuously as they were superfused with acetylcholine, carbamylcholine, methacholine, bethanechol, or physostigmine. Resting stress during stretch, acetylcholine-stimulated active stress, and total stress were determined. Proximal circular muscle was five times as sensitive to acetylcholine as distal circular muscle (p less than 0.05); proximal longitudinal muscle was 2.8 times as sensitive to bethanechol as distal muscle (p less than 0.05). Resting, active, and total stress were similar in proximal and distal muscle, but circular muscle showed nearly twice the resting stress of longitudinal muscle at either proximal or distal sites (p less than 0.05). Physostigmine (10(-6) M) increased acetylcholine-stimulated active stress in proximal and distal circular muscle by 29% and 70%, respectively (p less than 0.05), but not in longitudinal muscle (p greater than 0.05). This difference between proximal and distal circular muscle (41%) was also significant (p less than 0.05). Thus, the proximal and distal muscle of the rat small intestine differs in its sensitivity to various cholinergic agonists, but not in its length-stress properties.

Acetylcholine↗
PubMed1986

Bethanechol increases the diagnostic yield in patients with esophageal chest pain.

The diagnostic yield of routine esophageal manometrics in evaluating noncardiac chest pain is low. To determine if bethanechol stimulation would increase the diagnostic yield, we examined 87 patients with chest pain but no gastroesophageal reflux, 47 patients with gastroesophageal reflux but no chest pain, and 20 normal subjects. All subjects underwent standard esophageal manometrics before and after two doses of 50 micrograms/kg body wt bethanechol administered subcutaneously 15 min apart. Mean amplitude and duration of contractions and percentage of abnormal contractions were measured in the distal 7 cm of the esophageal body. Pathologic manometric parameters were defined as mean +/- 2 SD of values obtained in normal patients. Patients with chest pain had pathological responses for amplitude of contraction, duration of contraction, and percentage of abnormal contractions of 31%, 14%, and 22%, respectively, in the basal period. This increased to 43%, 66%, and 40%, respectively, after the first dose of bethanechol and to 53%, 85%, and 82% after the second dose of bethanechol. Chest pain was reproduced with new manometric abnormalities in 46% of patients after the first dose of bethanechol and in 77% after the second dose. Our conclusions are that: sequential bethanechol administration significantly increases the diagnostic yield of standard esophageal manometrics in the evaluation of noncardiac chest pain and duration of contraction after pharmacologic provocation with bethanechol is the best parameter to segregate patients with chest pain from normal subjects and gastroesophageal reflux patients.

Adult↗
PubMed1985

The effect of cholinergic agonists on coronary flow rate and oxygen consumption in isolated perfused rat heart.

The metabolic and circulatory consequences of activation of the muscarinic receptor(s) were investigated by local administration of acetylcholine and its three analogues (bethanechol, carbachol and methacholine) into beating and KCl-arrested perfused rat hearts. Acetylcholine and the three other choline esters caused vasoconstriction in both types of preparations and this vasoconstriction was accompanied by a decrease in oxygen consumption. In most cases the dose-response curves were biphasic and changes in coronary flow paralleled those in oxygen consumption. Both phenomena were abolished by administration of atropine and either removal of calcium or infusion of verapamil but were unaffected by addition of the adrenergic alpha-blocker, prazosin, and the adrenergic beta-blocker, propranolol. Infusions of low concentrations of the cholinergic agonists were accompanied by increases in the myocardial phosphorylation state ratio [( ATP]free/[ADP]free[Pi]) which correlated with the simultaneous decreases in oxygen consumption and coronary flow. It is suggested that muscarinic receptors responsible for vasoconstriction in perfused rat heart are located not only on coronary vessels but also on the cardiac muscle cells. Activation of the former receptors induces vasoconstriction by direct action on the vascular smooth muscle while activation of the latter receptors induces vasoconstriction indirectly by decreasing cardiac work and increasing the myocardial [ATP]free/[ADP]free[Pi] ratio. The results also show that stimulation of muscarinic receptor(s) and the consequent metabolic and vasoregulatory responses are coupled to calcium movements.

Animals↗