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At least 1,225 records · Page 68Linked to original sources
PubMed1984

The classification of adrenoceptors and their effects on gastric acid secretion.

The actions of adrenoceptor agonists and antagonists are by no means agreed even though experiments with adrenal medulla extract date back to the beginning of the century. This review will consider the work of my own group and that of others in an attempt to classify the adrenoceptors which modulate gastric acid secretion. There are a number of factors to consider. Species differences are important and particular attention will be given to results from rat, dog and human. The secretagogue used is also important because the effect of adrenoceptor agonists and antagonists can be modified by the choice of histamine, muscarinic agonist, (penta) gastrin or food. Other factors include the gastric model used and the presence or absence of anaesthesia. The broad conclusions are that both alpha- and beta-adrenoceptors can inhibit gastric acid secretion. Both beta 1- and beta 2-adrenoceptors mediate inhibition of pentagastrin-induced secretion while alpha-adrenoceptors are important in the reduction of histamine-induced gastric acid secretion.

Adrenergic alpha-Antagonists↗
PubMed1984

Adrenergic influence on gastric mucosal blood flow in gastric fistula dogs.

The aim of this study was to examine the influence of alpha-, beta- and dopaminergic receptors on gastric mucosal blood flow during "high", "normal", and "low" vagal conditions obtained by stimulation with bethanechol and pentagastrin and by parietal cell vagotomy respectively. During pentagastrin and bethanechol stimulation, a linear relationship between gastric acid secretion and mucosal blood flow was observed. During pentagastrin stimulation, dopamine (40 micrograms/kg/min) did not change the blood flow values while a decrease in acid secretion was found. During bethanechol stimulation dopamine (10 micrograms/kg/min) induced an increase in mucosal blood flow and a similar increase in acid secretion. If the dopamine infusion was preceded by alpha-receptor blockade, a pronounced increase in mucosal blood flow was observed without a similar increase in acid secretion. beta-adrenergic stimulation (isoprenaline) reduced the pentagastrin and bethanechol stimulated gastric acid secretion without a similar decrease in mucosal blood flow. beta-blockade (propranolol) increased the pentagastrin stimulated gastric acid secretion in parietal cell vagotomized dogs. This increase in acid output was preceded by an initial increase in mucosal blood flow and in the last two periods a decrease in blood flow. alpha-Blockade (phentolamine) reduced the pentagastrin stimulated gastric acid secretion and gastric mucosal blood flow but the ratio between blood flow and acid secretion was increased, indicating a relatively increasing effect on mucosal blood flow. One may conclude that blood flow and acid secretion are not unconditionally linked and that at least two different mechanisms are involved in blood flow changes in the stomach.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Dopaminergic and beta-adrenergic effects on gastric antral motility.

Stimulation of splanchnic nerves and application of adrenergic drugs have been shown to give variable effects on gastric motor activity depending especially on the background activity. beta-adrenoceptors and dopaminergic receptors mediate inhibitory effect on proximal gastric motor activity. The purpose of the present study was to evaluate the effects of isoprenaline, a beta 1- and beta 2-agonist, and dopamine on gastric antral motility in gastric fistula dogs. Dopamine was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors during infusion of bethanechol or pentagastrin inducing motor activity patterns as in the phase III of the MMC and the digestive state respectively. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by specifically acting dopaminergic blockers, while alpha- and beta-adrenergic blockers were without any significant effects. Dose-response experiments with bethanechol and dopamine showed inhibition of a non-competitive type. Isoprenaline was used alone and in conjunction with selective blockade of beta 1- and beta 2-receptors during infusion of bethanechol which induces a pattern similar to phase III in the migrating myoelectric complex. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect could be significantly blocked by propranolol (beta 1 + beta 2-adrenoceptor blocker) and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. The dose-response experiments showed inhibition of a non-competitive type. These studies indicate that gastric antral motility is inhibited by isoprenaline through both beta 1- and beta 2-receptors and by dopamine through specific dopaminergic receptors.

Adrenergic beta-Agonists↗
PubMed1984

Control of gastroduodenal coordination: dopaminergic and cholinergic pathways.

The efficacies of the gastrokinetic drugs domperidone, cisapride , metoclopramide and bethanechol to improve antroduodenal coordination were compared in two test systems: in vitro, the gastroduodenal preparation of the guinea-pig; in vivo, the conscious dog implanted with strain gauges on antrum and duodenum. Antroduodenal coordination could be quantified for both the in vitro and in vivo systems. Drug effects were similar for both test models. Domperidone and cisapride , and to a lesser extent metoclopramide but not bethanechol, effectively improved antroduodenal coordination indicating that both dopaminergic and cholinergic pathways modulate antroduodenal motor patterns.

Animals↗
PubMed1984

Pancreatic polypeptide release: role of stimulants of exocrine pancreatic secretion in dogs.

There are apparent similarities in the mechanisms of the intestinal phase of exocrine and pancreatic polypeptide (PP) secretion by the pancreas. To characterize this relationship, we measured incremental responses of protein, bicarbonate, and PP to graded doses of intravenous secretin, caerulein, CCK8, CCK33, bethanechol, and intraduodenally perfused HCl, sodium oleate, and L-phenylalanine in dogs with gastric and pancreatic fistulas and compared them with average postprandial values. Secretin did not release PP at any dose studied, whereas intraduodenal HCl increased PP levels slightly at a load maximal for pancreatic secretion. Caerulein produced dose-related increases in PP secretion (maximal, 106% of meal response) but CCK8 and CCK33 had much less effect at doses equivalent for protein secretion. Bethanechol was a weak stimulant for PP only at the largest tolerable dose. L-Phenylalanine and sodium oleate markedly increased protein secretion, but only oleate clearly stimulated PP. Our results suggest a greater quantitative importance of the intestinal phase for exocrine than endocrine (PP) pancreatic secretion.

Animals↗
PubMed1984

Mechanical trauma to bladder epithelium liberates prostanoids which modulate neurotransmission in rabbit detrusor muscle.

Transitional epithelium of the rabbit urinary bladder has been implicated as a major site of prostanoid production and various studies have indicated that prostanoids have significant influences in muscle activity and neurotransmission in the bladder. We have examined the possibility that mechanical irritation of the epithelium could release diffusable substances which could influence neuromuscular function in the bladder. Epithelium was dissected from muscle strips of rabbit urinary bladder and the two components were incubated in separate chambers. Krebs' solution bathing epithelium was transferred to the bath in which the muscle was being field stimulated. Increases in the basal tension and spontaneous activity of the muscle as well as in the electrically evoked responses were observed after transfer and were related to the intensity of the irritation given the epithelium sample. The effects were mimicked by prostaglandins E1 E2, F2 alpha and I2 and the transfer effect was reduced significantly by pretreatment of the epithelium, but not the muscle, with indomethacin (10 microM) or ibuprofen (100 microM). Transfer of solution bathing-irritated epithelium also raised basal tension but not the maximum response to bethanechol. Finally, radioimmunoassay was used to demonstrate that irritation of epithelium samples caused the appearance of prostaglandin and 6-oxo-prostaglandin F1 alpha in the bathing medium and that this appearance was profoundly depressed by indomethacin (10 microM). It is plausible, therefore, that mechanical irritation of the bladder epithelium could result in changes in neuromuscular function in the underlying muscle layers and that these changes would be consistent with the symptoms associated with mechanical trauma of urothelium.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

An experimental model to perform dynamic studies of exocrine pancreatic secretion in mice.

An experimental model to perform dynamic studies of exocrine pancreatic secretion from mice has been developed. It consists of a microsurgical procedure in anesthetized mice using a stereoscopic microscope. The bile-pancreatic common duct was individualized, isolated and cannulated. A specially calibrated capillary tube was placed in the free end of the cannula and put on a millimetrical rule. Readings of pure pancreatic juice flow rate were performed minute by minute to obtain a flow rate curve. The procedure allowed the discrimination among increasing betanechol doses of 0.1, 0.2, and 0.4 microgram/g body weight.

Animals↗
PubMed1984

Management of reflux esophageal disease.

Although frequent or prolonged exposure of the esophageal mucosa to gastric contents results in epithelial damage, it is also becoming clear that the pathophysiology of reflux esophageal disease may be multifactorial. The severity of this disease may relate to the frequency of reflux episodes, certainly to the duration of mucosal exposure to refluxed material, and probably to as yet unquantified factors of mucosal resistance and the specific noxiousness of refluxed gastroduodenal and pancreatic secretions. The phenomenon of esophageal clearance is a critical determinant in preservation of mucosal integrity, and a disturbance in this function may lead to severe signs and symptoms of reflux esophageal disease. A detailed analysis of the specific pathophysiologic abnormalities in individual patients may permit more "tailored" therapeutic approaches and more favorable results.

Bethanechol Compounds↗
PubMed1981

A comparison of cyclic guanosine 3':5'-monophosphate and muscarinic excitatory responses in the superior cervical ganglion of the rat.

The relationship between the magnitude of atropine-sensitive afterdischarge (AD), which is generated from slow excitatory postsynaptic potentials and the ganglionic cyclic guanosine 3':5'-monophosphate (cGMP) concentration was investigated in the rat superior cervical ganglion in vitro. Parallel increases in the magnitude of atropine-sensitive AD and cGMP concentration occurred with increasing frequency of preganglionic nerve stimulation up to 40 Hz for 10 sec. However, AD was completely antagonized by atropine, 0.1 to 1 microM, whereas the cGMP response was not significantly affected by up to 25 microM atropine. Although bethanechol, 0.5 mM, causes an asynchronous firing which can be recorded from the postganglionic nerve, bethanechol had no effect on the ganglionic cGMP concentration even in ganglia preincubated with the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, 1 mM. The methylxanthine did increase the resting cGMP concentration and the concentration of cGMP immediately after stimulation of the preganglionic nerve. It is concluded that muscarinic AD and the slow excitatory postsynaptic potentials of rat sympathetic ganglia are not generated by a mechanism involving an increase in ganglionic cGMP.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Pharmacologic identification, activation and antagonism of two muscarine receptor subtypes in the lower esophageal sphincter.

Lower esophageal sphincter pressures were monitored with water-filled catheters in anesthetized opossums. Muscarinic agonists McN-A-343 and bethanechol were administered in the arterial supply of the sphincter. McN-A-343 caused relaxation after a brief contraction of the sphincter. Bethanechol caused a dose-dependent contraction. Tetrodotoxin antagonized the inhibitory effect of McN-A-343 but did not antagonized sphincter contraction caused by McN-A-343 or bethanechol. The mean ED50 values were 6.9 nmol/kg i.a. for McN-A-343-induced relaxation, 10.5 nmol/kg i.a. for McN-A-343-induced contraction and 0.4 nmol/kg i.a. for bethanechol-induced contraction. Atropine caused a dose-dependent rightward shift in the dose-response curves of inhibitory and excitatory effects of the two muscarinic agonists. Pirenzepine caused a dose-dependent rightward shift in the dose-response curves of McN-A-343-induced relaxation. Pirenzepine did not modify sphincter contraction caused by the muscarinic agonists. 4-Diphenylacetoxy-N-methylpiperidine methiodide, on the other hand, did not modify McN-A-343-induced sphincter relaxation but caused dose-dependent rightward shifts in the dose-response curves of sphincter contraction caused by McN-A-343 or bethanechol. These studies suggest that there are two distinct types of muscarine receptors in the opossum lower esophageal sphincter. The M1 muscarine receptors are present on the inhibitory neurons and participate in the synaptic transmission between vagal preganglionic and intramural postganglionic inhibitory neurons. They are activated by McN-A-343 and antagonized by pirenzepine. The M2 muscarine receptors are located directly on the sphincter muscle. They are also activated by McN-A-343, but are selectively activated by bethanechol and are antagonized by 4-diphenylacetoxy-N-methylpiperidine methiodide.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1980

Cholinergic, adrenergic and purinergic response of sequential strips of rabbit urinary bladder.

In this study, we have characterized the response of five sequential segments of urinary bladder to cholinergic, adrenergic, and purinergic agonists. The results indicate that an abrupt alteration in pharmacological response between bladder body and base occurs at the level of the ureteral orifices. The bladder body responds preferentially to urecholine (muscarinic cholinergic), isoproterenol (beta adrenergic) and ATP (purinergic), whereas the bladder base responds perferentially to methoxamine alpha adrenergic). In parallel studies, the density of both muscarinic cholinergic receptors ([3H]quinuclidinyl benzilate binding sites) and beta adrenergic receptors were significantly higher in the body than in the base, whereas the concentration of alpha adrenergic receptors was greater in the bladder base than in the body. From these studies, we conclude that the differences in the response of the bladder base and body to cholinergic and adrenergic agents are primarily due to differences in the densities of the specific autonomic receptors. In addition, the response of the bladder to ATP (which is a putative neurotransmitter in the urinary bladder) can also be separated between body and base. The distribution is similar to that observed for urecholine.

Adenosine Triphosphate↗
PubMed1981

Influence of papaverine on bethanechol or OP-CCK stimulation of feline colonic muscle.

Papaverine relaxes smooth muscle from various organ systems throughout the body. The purpose of this study was to determine the effects of papaverine on colonic smooth muscle from the transverse colon of the cat. Myoelectrical activity was recorded with monopolar glass pore electrodes. Papaverine was administered alone and simultaneously with bethanechol or the octapeptide of cholecystokinin. Higher concentrations of papaverine (10(-4) M, 10(-5) M) abolished both slow-wave activity and migrating spike bursts. Lower concentrations of papaverine (10(-6) M) had no effect on slow waves or the migrating spike burst. Bethanechol (10(-6) M) or OP-CCK (4 x 10(-9) M, 4 x 10(-10) M) stimulated spike activity (p < 0.001). Papaverine (10(-6) M had a minimal effect on the increase in spike activity that occurred after octapeptide of cholecystokinin in a concentration of 4 x 10(-10) M (p < 0.05). Papaverine had no effect on the stimulation of the colonic smooth muscle by 4 x 10(-10) M octapeptide of the colonic smooth muscle by 4 x 10(-9) M octapeptide of cholecystokinin. These studies show that (a) papaverine can inhibit smooth muscle myoelectrical activity, (b) papaverine is a potent inhibitor of cholinergic stimulation of colonic smooth muscle, but (c) papaverine has a minimal effect on octapeptide of cholecystokinin stimulation of the isolated colonic smooth muscle.

Animals↗
PubMed1978

Neurologic control of prostatic secretion in the dog.

A model to record the volume of prostatic secretion was developed. The influence of both divisions of the autonomic nervous system on the prostate by pharmacologic stimulation and blockade, and by direct electrical nerve stimulation was observed. The prostate responded to parasympathetic stimulus by increasing secretion. Under sympathetic stimulation, the secretion collected in the acini and ducts was expulsed into the urethra by contraction of the smooth muscle fibers surrounding these structures. A correlation between these findings and the normal sexual function may be made: Early in the excitation phase there is parasympathetic activity with increased secretion. With onset of orgasm and emission, sympathetic activity initiates the contractile activity of the genital duct system and the prostatic muscular element. As a result, the secretion is transported to the prostatic urethra (emission) to be later ejaculated by the genital skeletal musculature of the perineum, mainly the ischiocavernosus and bulbospongiosus.

Angiotensin II↗