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PubMed1988

Muscarinic receptor interaction with full and partial beta-adrenoceptor agonists in the rat colon strip.

beta-Adrenoceptor agonists inhibit contractile activity in isolated colon strips. In order to demonstrate that beta-adrenoceptors are located at different functional levels within the colon wall, increasing concentrations of muscarinic agonists were used to interact functionally with the beta-adrenoceptor-mediated inhibition of spontaneous colon activity. The effects of the full agonists isoprenaline and terbutaline and of the partial agonist prenalterol were functionally antagonized by carbachol (0.03 and 0.3 mumol/l) and bethanechol (1.3 and 30 mumol/l). This functional antagonism was parallelled by an increase in baseline tension and spontaneous contractile activity of the isolated colon strip. At lower concentrations of carbachol (0.003 and 0.01 mumol/l) or bethanechol (0.03 and 0.3 mumol/l) no effect on the contractile status of the smooth muscle or on the pD2-values of the full agonists was seen. However, at these lower concentrations of muscarinic agonists a marked decrease in the maximal inhibitory response to the partial beta-adrenoceptor agonist prenalterol was demonstrated. The inhibitory response to prenalterol showed a biphasic concentration-response curve. The muscarinic antagonist atropine produced an increase in the maximal response of the high potency component of the concentration-response curve for prenalterol and an increase in the sensitivity to isoprenaline. These results demonstrate the presence of a high cholinergic tone in the colon preparation of a magnitude that clearly reduces the sensitivity to beta-adrenoceptor agonists. The different responses to full and partial beta-adrenoceptor agonists in the presence of increasing concentrations of muscarinic agonists may indicate that beta-adrenoceptors are located on two different functional units within the colon wall.

Adrenergic beta-Agonists↗
PubMed1987

The effects on Schild regressions of antagonist removal from the receptor compartment by a saturable process.

A theoretical model of the effects of a saturable removal mechanism for an antagonist diffusing into the receptor compartment of a tissue is used to calculate expected deviations in Schild regressions. At concentrations of antagonist which do not saturate the removal mechanism, there can be a deficit of antagonist in the receptor compartment as compared to the concentration of antagonist bathing the tissue. This results in a shift to the right of the Schild regression and a corresponding underestimation of antagonist potency. The model predicts that as the concentration of antagonist exceeds the Km for removal (saturation of the removal process), this concentration deficit is eliminated, resulting in a proportionate increase in antagonist concentration at the receptor and a concomitant increase in receptor antagonism. This results in a steepening of the Schild regression; the slope in the region of saturation is greater than one. Experimental evidence in support of this model was found in studies of the antagonism of responses to bethanechol by atropine in rabbit ileum; this species is known to have an atropinesterase capable of hydrolyzing atropine. The Schild regression for atropine was curvilinear with an overall slope of 1.42 (1.34-1.5) and pKB = 8.5 (8.36-8.8); in the ileum from guinea pigs, a species which does not possess this enzyme, the Schild regression for atropine was linear, had a slope not significantly different from unity (1.1; 0.95-1.2) and a pKb of 9.0 (8.9-9.2). The slope of the regression in rabbit ileum was corrected to unity by the addition of an excess concentration of methylbutyrate, an alternate substrate for atropinesterase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Cytological effects of urecholine stimulation on the rat pancreas.

Stimulation of the exocrine pancreas by the secretagogue urecholine caused degranulation of the acinar cells. Under in vivo conditions, this degranulation is not uniform throughout the tissue. Indeed some of the acini are almost completely depleted of their granules while others display the appearance of resting acini. A noticeable feature is that all the cells of the same acinus display a comparable degree of degranulation. Moreover, groups of neighbouring acini seem to respond simultaneously suggesting that the secretory stimulus is propagated from one acinus to the other. In vitro stimulation of dispersed acini also showed that some of the acini are more responsive than others indication that this phenomenon can not be attributed to accessibility of the secretagogue to its receptor. These observations lead us to accessibility of the secretagogue to its receptor. These observations lead us to the concept that the response of the pancreatic acinar cell is controlled at the level of the acinus.

Animals↗
PubMed1983

Localization and release of lysozyme from ferret trachea: effects of adrenergic and cholinergic drugs.

Lysozyme is a bacteriolytic enzyme found in respiratory tract fluid. In this study, immunocytochemistry was used to determine the cells of origin of tracheal lysozyme in the ferret. Lysozyme was found in secretory granules of serous but not mucous cells in the submucosal glands, and was absent from the surface epithelium, cartilage, and connective tissue. The exclusive presence of lysozyme in serous gland cells renders it useful as a biochemical marker of that cell type. Measurements of lysozyme assayed from the incubating medium indicated that bethanechol stimulated lysozyme release by 260 +/- 80.9% (mean +/- SE), phenylephrine by 80 +/- 16.4%, and terbutaline by 25 +/- 10.2%. Electron-microscopic and immunocytochemical analysis of incubated tissues revealed loss of serous granules and lysozyme immunoreactivity in response to the drugs. Atropine, propranolol, and phentolamine blocked the stimulatory effects of bethanechol, terbutaline, and phenylephrine, respectively. These findings establish the usefulness of lysozyme as a serous-cell marker and demonstrate that secretory responses of different magnitude are evoked by equimolar concentrations of alpha- and beta-adrenergic and cholinergic drugs.

Animals↗
PubMed1988

Dissociation of the metabolic from the contractile response to muscarinic stimulation in the rabbit urinary bladder.

The calcium dependence of contraction and NADH fluorescence was investigated in rabbit bladder stimulated with bethanechol or KCl. The absence of calcium in the bathing solution induced a rightward shift in the dose response to bethanechol for both contraction and NADH fluorescence. The contractile response was shifted to a greater degree than the fluorescence response and the maximal response to bethanechol was reduced by 80% for contraction but only 20% for NADH fluorescence. This rightward shift was also induced by the benzothiazepine calcium antagonist diltiazem (200 microM) and again the contractile response was shifted significantly more than the fluorescence response. The combination of zero calcium and 200 microM diltiazem virtually abolished contractions but only inhibited the NADH fluorescence by 65% at maximally effective bethanechol concentrations. Unlike the effect of diltiazem on the response to bethanechol, diltiazem (200 microM) shifted both the contraction and fluorescence curves to the right equally in response to KCl stimulation. These results indicate that a metabolic response to muscarinic stimulation (decreased NADH) can occur in the absence of any observable contractile response. This metabolic response may be due to post receptor signal processing events. For KCl stimulation, the NADH response is probably secondary to and a result of the contractile response.

Animals↗
PubMed1977

Effects of cytochalasin B on pancreatic acinar cell structure and secretion.

The effects of cytochalasin B (CB) on pancreatic structure and amylase release were studied by use of pancreatic fragments, isolated acini and isolated acinar cells. In pancreatic fragments and isolated acini CB caused the disappearance of microfilaments underlying the apical plasma membrane, loss of apical microvilli and luminal swelling, the last of which was greatly enhanced by addition of protein secretagogues. CB had no effect on basal amylase release but inhibited bethanechol-stimulated amylase in both fragments and acini. Isolated acinar cells, while retaining overall polarity, had lost most of the apical specialization including the microfilament and microvillous complex. Cells were still able to release amylase in response to bethanechol but this release was not affected by CB. The only structural effect of CB on isolated cells was margination of zymogen granules against the plasma membrane. This was, however, not accompanied by increased amylase release. It is concluded that microfilaments are important in maintaining the pancreatic acinar structure. Interference with this structure by CB leads to inhibition of bethanechol-stimulated amylase release. Microfilaments, however, may not play a direct role in secretion.

Amylases↗
PubMed1978

Catharanthine: a novel stimulator of pancreatic enzyme release.

The plant alkaloid, catharanthine, was shown to stimulate release of amylase from pancreatic fragments and to cause extensive degranulation of pancreatic acinar cells with accumulation of membrane material in the Golgi region. The extent and time course of maximal catharanthine stimulation was comparable to that induced by the cholinergic analog bethanechol. Antimycin inhibited the action of catharanthine while atropine did not. Removal of Ca2+ from the incubation medium inhibited amylase release induced by catharanthine but did not affect release induced by bethanechol. Catharanthine induced a delayed release of 45Ca2+ from prelabeled pancreatic fragments as compared to bethanechol. It is suggested therefore that catharanthine activates the physiological pathway controlling amylase release by causing a rise in cytoplasmic Ca2+ but the mechanism by which this occurs is different from that caused by physiological secretagogues.

Amylases↗
PubMed1984

Cytological effects of ionophore-induced stimulation on the exocrine pancreas of the rat.

Rat-pancreas lobules were incubated with the ionophore A-23187 in the presence of Ca2+. After 90 min, some of the acini were partially or almost completely depleted of their zymogen granules while others had the appearance of resting acini. With few exceptions, the cells of a given acinus were degranulated to a comparable level. Slight dispersion of the zymogen granules was noticed in cells incubated in a Ca2+-free medium containing EGTA with or without A-23187. In the presence of Ca2+ the secretory response obtained with the ionophore was comparable to that observed with 10(-5)M urecholine. The results obtained provide cytological evidence that the secretory response is only partially determined at the membrane-receptor level and that other mechanisms intervene between cytosol Ca2+ increase and exocytosis.

Amylases↗
PubMed1991

Creatine kinase activity in normal and hypertrophied rabbit urinary bladder tissue (following partial outlet obstruction).

The urinary bladder depends on intracellular ATP to support a number of essential intracellular processes including contraction. The concentration of ATP is maintained by mitochondrial oxidative phosphorylation, cytosolic glycolysis and the cytosolic activity of creatine kinase, the enzyme that catalysis the rapid transfer of a phosphate from creatine phosphate (CP) to ADP resulting in the formation of ATP. Prior studies in this lab and others have demonstrated that mitochondrial respiration is significantly lower in hypertrophied bladder tissue (induced by partial outlet obstruction of the white New Zealand Rabbit). In addition to decreased mitochondrial respiration, there are significant increases in glycolysis and lactic acid formation in the hypertrophied tissue. In view of the increased glycolysis and decreased mitochondrial function in the hypertrophied tissue, and the importance in creatine kinase in maintaining cytosolic levels of ATP, the current study was designed to determine if outlet obstruction induces any changes in the activity of creatine kinase. The following is a summary of the results: 1) The bladder mass increased from 2.2 +/- 0.2 gm to 11.5 +/- 1.6 gm at 7 days following outlet obstruction. 2) The intracellular concentrations of both ATP and CP were significantly reduced in the bladder tissue following 7 days of obstruction. 3) The percent of protein (per tissue mass) was significantly lower in the obstructed bladders, although the percent of soluble protein was similar. 4) Creatine kinase activity of control bladders showed linear kinetics with a Vmax = 1120 nmoles/mg protein/4 min and Km = 147 microM CP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1978

Denervation supersensitivity of the urethra to alpha-adrenergics in the chronic neurogenic bladder.

The response of the urethral pressure profile to the administration of various autonomic drugs was compared between a group of eight patients with chronic neurogenic bladder as evidenced by denervation supersensitivity to besacholineR and a group of 10 control subjects. A supersensitive response to the administration of an alpha-stimulant with a rise of maximum urethral pressure of 10 mmHg or more above the control urethral pressure was uniformly observed in the urethra of patients with chronically denervated bladders. Mechanisms of supersensitivity are postulated and the significance of alpha-adrenergic innervation of the urethra are stressed. These results appear to add pharmacological evidence of alpha-adrenergic predominance in the urethra which is now believed to be dually innervated.

Bethanechol Compounds↗
PubMed1983

Analysis of the anticholinergic and musculotropic effects of desmethylimipramine on the rabbit urinary bladder.

The anticholinergic and musculotropic relaxant properties of desmethylimipramine (DMI) on smooth muscle were investigated utilizing cholinergic radioligand receptor binding and in-vitro muscle bath techniques. Receptor binding studies revealed the direct antimuscarinic potency of DMI to be 1/480th that of atropine. Muscle bath studies characterized discrete antimuscarinic and musculotropic actions. An initial, competitive antimuscarinic action could be separated from a delayed onset, noncompetitive musculotropic action by altering the time between the addition of DMI and the addition of bethanechol to the smooth muscle bath.

Animals↗
PubMed1981

Effect of vasoactive intestinal peptide on the contractility of the rabbit urinary bladder.

Vasoactive intestinal peptide (V. I. P.) has been demonstrated in neuronal elements of smooth muscle organs including the urinary bladder, thus indicating that this peptide may be a neurohumoral transmitter. In isolated strips of rabbit urinary bladder we have demonstrated that V. I. P. causes relaxation. Unlike the relaxant effect of the beta agonist isoproterenol, the inhibition produced by V. I. P. could not be blocked by propranolol. These studies indicate that V. I. P. may play a role in the regulation of bladder contractility.U

Animals↗
PubMed1980

The action of bromocriptine on human detrusor muscle.

The pharmacological effects of bromocriptine on human detrusor muscle were investigated by an in vitro isometric method. Both a direct stimulating effect and an anticholinergic effect were demonstrated. These effects, together with an alpha-adrenergic blocking effect reported in a previous paper, are correlated with the published clinical effects of bromocriptine in patients with primary and secondary unstable detrusors.

Bethanechol Compounds↗
PubMed1989

Evidence for a respiration-modulated cholinergic action on the activity of medullary respiration-related neurons in the rabbit. An iontophoretic study.

Effects of the iontophoretically administered cholinergic agonists acetylcholine, bethanechol and DMPP on the activity of medullary respiration-related neurons were examined in urethane-anaesthetized rabbits. Inhibitory effects prevailed over excitatory effects. Analysis of cholinergic effects by cycle-triggered averaging revealed three major types of neuronal responses: (i) constant alterations of spike-density throughout the whole period of activity ("constant effects"), (ii) effects increasing during the progression of the burst of discharge or effects restricted to a particular fraction of the burst ("phasic effects") and (iii) effects which were characterized by an excitation during one respiratory phase and an inhibition during the other phase ("bi-phasic effects"). The latter type of effects was observed in phase-spanning respiration-related neurons. Phasic effects were mainly observed in inspiration-related neurons which were predominantly inhibited by stimulation of muscarinic receptors. Inspiratory R beta-neurons in no case were phasically affected by cholinergic agents. The mean muscarinic inhibition of inspiration-related neurons increased with the progression of inspiration. The mean nicotinic inhibition of expiration-related neurons decreased with the progression of expiration. Results suggest that the efficacy of (i) a central inspiration terminating mechanism and (ii) the onset of discharge of expiratory neurons is modulated by acetylcholine.

Acetylcholine↗
PubMed1993

Galanin activates an inwardly rectifying potassium conductance in mudpuppy atrial myocytes.

Galanin- and bethanechol-activated K+ currents have been studied in mudpuppy atrial myocytes. The galanin and bethanechol K+ currents were time-dependent and inwardly rectifying. In GTP gamma S, the galanin and bethanechol currents were reduced progressively as G-protein gated K+ channels became activated. GDP beta S inhibited agonist-induced outward currents. We conclude that galanin and bethanechol activate the same or a very similar inwardly rectifying K+ conductance and that activation of a G protein is required.

Animals↗
PubMed1992

Tetraethylammonium blocks muscarinically evoked secretion in the sheep parotid gland by a mechanism additional to its blockade of BK channels.

Since the secretory cells of the sheep parotid gland contain large numbers of high-conductance, voltage- and Ca(2+)-activated K+ channels (BK channels), we have used tetraethylammonium (TEA), a commonly employed blocker of BK channels, to investigate their role in secretion by this gland. In patch-clamp studies we found that 10 mmol/l TEA applied extracellularly inhibits the BK channel but not a 30-pS K+ channel also seen in this gland. We then showed by in-vivo perfusion that muscarinically evoked secretion is inhibited almost completely by 10 mmol/l TEA. We next used microspectrofluorimetry with fura-2 to demonstrate that muscarinic agonists cause the intracellular free Ca2+ concentration to increase. Unexpectedly, however, we found that 0.3-10 mmol/l TEA inhibited the increase in intracellular free Ca2+ induced by 5.0 mumol/l bethanechol or by 0.1 mumol/l acetylcholine. Consequently we conclude that the inhibition of muscarinically evoked secretion by the sheep parotid gland by TEA cannot be attributed solely to blockade of the BK channel--rather it must be attributed, at least in part, to blockade of some step in muscarinic signal transduction, for instance, receptor-agonist binding or Ca2+ release into the cytosol.

Animals↗