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PubMed1980

Supersensitivity to prostaglandin in chronic neurogenic bladders.

The bladder response to prostaglandin (PG test) was investigated in chronic neurogenic bladders by isometric cystometry and compared with the results obtained from normal subjects. The urinary bladder was filled with 100 ml of saline and 100 micrograms of prostaglandin 995 were injected intravenously. The changes in bladder and intra-abdominal pressures were observed for up to 20 min. A rise in detrusor pressure of more than 20 cm of water was judged a positive response. Out of 21 neurogenic bladders 12 had a positive response. The result of the PG test demonstrated a good correlation with the supersensitivity test to bethanechol chloride which was performed on these patients on a different day. All of the normal subjects had negative responses. It was concluded that the chronically denervated bladder is supersensitive to prostaglandin 995.

Adolescent↗
PubMed1981

Bladder transection--a functional, neurophysiological, neuropharmacological and neuroanatomical study.

Experimental models to represent the surgical methods of bladder transection in humans were performed on dogs and rabbits. The effects on vesical neurophysiology were studied by cystometry with bethanechol supersensitivity testing; by in vitro pharmacological responsiveness; by determination of autonomic receptor densities using radioligand binding and by autonomic neurohistochemical staining. Analysis revealed that transection with or without neurovascular preservation resulted in an alpha-adrenergic denervation and cholinergic decentralisation. A comparison with the surgical models is presented and proposed mechanisms of action are discussed in relation to the experimental results.

Animals↗
PubMed1982

Neuropathic vesicourethral dysfunction in children. A trial comparing clean intermittent catheterisation with manual expression combined with drug treatment.

Forty-three children with overt neurological disease and neuropathic vesicourethral dysfunction were entered into a trial comparing clean intermittent catheterisation (CIC) with manual expression combined with drug treatment (non-CIC). The 22 children in the CIC group showed a significantly greater improvement in continence than the 21 children in the non-CIC group (P less than 0.001) without a significant increase in the incidence of urinary tract infections. Neither form of treatment is effective in reducing the risk of deterioration of renal function due to the combination of detrusor-sphincter dyssynergia and vesicoureteric reflux. Neither form of treatment improves continence in the presence of gross sphincter weakness or gross impairment of bladder compliance.

Bethanechol Compounds↗
PubMed1986

Acute dystonic reaction to bethanechol--a direct acetylcholine receptor agonist.

Bethanechol is a direct agonist of the acetylcholine receptor that was recently introduced in the therapy of gastro-oesophageal reflux. Acute dystonic reactions to bethanechol were observed in a 10-month-old infant who also demonstrated similar dystonic reactions to dopamine receptor blocking agents of two different classes. This first report of acute dystonic reaction to cholinergic agonists in human is in accord with the current theories of the rôle of acetylcholine and dopamine in the pathogenesis of acute dystonic reactions.

Acute Disease↗
PubMed1984

Activation of tyrosine hydroxylase in the superior cervical ganglion by nicotinic and muscarinic agonists.

Both dimethylphenylpiperazinium (DMPP), a nicotinic agonist, and bethanechol, a muscarinic agonist, increase 3,4-dihydroxyphenylalanine (DOPA) synthesis in the superior cervical ganglion of the rat. DMPP causes approximately a fivefold increase in DOPA accumulation in intact ganglia whereas bethanechol causes about a two-fold increase in DOPA accumulation. These effects are additive with each other and with the increase in DOPA accumulation produced by 8-bromo cyclic AMP. The action of DMPP is dependent on extracellular Ca2+ while the actions of bethanechol and 8-bromo cyclic AMP are not dependent on extracellular Ca2+. Cholinergic agonists and cyclic nucleotides produce a stable activation of tyrosine hydroxylase (TH) in the ganglion. The activation of TH by nicotinic and muscarinic agonists can be detected after 5 min of incubation of the ganglia with these agents. The nicotinic response disappears after 30 min of incubation, whereas the muscarinic response persists for at least 30 min. The Ca2+ dependence of the TH activation produced by these agents is similar to the Ca2+ dependence of their effects on DOPA accumulation in intact ganglia. These data are consistent with the hypothesis that nicotinic agonists, muscarinic agonists, and cyclic AMP analogues increase TH activity by three distinct mechanisms. The activation of TH presumably underlies the increase in DOPA synthesis produced by these agents.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Regional differences in the coupling of muscarinic receptors to inositol phospholipid hydrolysis in guinea pig brain.

The differential effects of muscarinic agents on inositol phospholipid hydrolysis and the role in this process of putative muscarinic receptor subtypes (M1 and M2) were investigated in three regions of guinea pig brain. Addition of the agonist oxotremorine-M to slices of neostriatum, cerebral cortex, or hippocampus incubated in the presence of myo-[2-3H]inositol and Li+ resulted in a large accumulation of labeled inositol phosphates (733, 376, and 330% of control, respectively). In each tissue, the principal product formed was myo-inositol 1-phosphate (59-86%), with smaller amounts of glycerophosphoinositol and inositol bisphosphate. Only trace amounts of inositol trisphosphate could be detected. Regional differences were observed in the capacity of certain partial agonists to evoke inositol lipid hydrolysis, the most notable being that of bethanechol, which was four times more effective in the neostriatum than in either the cerebral cortex or hippocampus. In addition, the full agonists, oxotremorine-M and carbamoylcholine, were more potent stimulators of inositol phosphate release in the neostriatum than in the cerebral cortex. The putative M1 selective agonist 4-m-chlorophenylcarbamoyloxy-2-butynyl trimethyl ammonium chloride had little stimulatory effect in any brain region, whereas the putative M1 selective antagonist pirenzepine blocked the enhanced release of inositol phosphates with high affinity in the cerebral cortex and hippocampus (Ki = 12.1 and 13.9 nM; "M1") but with a lower affinity in the neostriatum (Ki = 160 nM; "M2"). In contrast to its differential effects on stimulated inositol lipid hydrolysis, no regional differences were observed in the capacity of pirenzepine to displace [3H]quinuclidinyl benzilate, a muscarinic antagonist, bound to membrane fractions. Atropine, an antagonist that does not discriminate between receptor subtypes, inhibited the enhanced release of inositol phosphates with similar affinities in the three regions (Ki = 0.40-0.60 nM). The results indicate that by measurement of inositol lipid hydrolysis, regional differences in muscarinic receptor coupling characteristics become evident. These differences, which are not readily detected by radioligand binding techniques, might be accounted for by either the presence of functionally distinct receptor subtypes, or alternatively, by regional variations in the efficiency of muscarinic receptor coupling to inositol lipid hydrolysis.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1990

Involvement of dihydropyridine-sensitive Ca2+ channels in adenosine-evoked inhibition of acetylcholine release from guinea pig ileal preparation.

The effects of adenosine and nifedipine on endogenous acetylcholine (ACh) release evoked by electrical stimulation from guinea pig ileal longitudinal muscle preparations exposed to physostigmine were evaluated using an HPLC with electrochemical detection (ECD) system. Resting ACh release, which was sensitive to tetrodotoxin (0.3 microM), was enhanced by Bay K 8644 (0.5 microM; a Ca2+ antagonist) or 4-aminopyridine (30 microM; a K+ channel blocker) but not by theophylline (100 microM; a P1 purinoceptor antagonist) or atropine (0.3 microM). The enhancement of the resting ACh release by Bay K 8644 was virtually unaffected by atropine. Electrically evoked ACh release was enhanced by around two- to fourfold in the presence of theophylline, atropine, Bay K 8644, 4-aminopyridine, or atropine. On the other hand, the evoked ACh release was reduced by adenosine (10-30 microM), nifedipine (0.1-0.3 microM; a dihydropyridine Ca2+ channel antagonist), or bethanechol (1-3 microM) in a concentration-related fashion. The reduction induced by adenosine or nifedipine was almost abolished by either theophylline or Bay K 8644, whereas that induced by bethanechol was virtually unaffected by these drugs. The inhibition by adenosine of ACh release was not influenced in the presence of 4-aminopyridine or atropine. However, this inhibition by adenosine was considerably enhanced by halving the Ca2+ concentration in the Krebs solution and was diminished by doubling the Ca2+ concentration. These findings suggest that adenosine produces a cholinergic neuromodulation presumably via modifying dihydropyridine-sensitive Ca2+ channel activities in the cholinergic neurons, and thus L-type Ca2+ channels may exist on the nerve terminals.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Contractile responses of tracheal smooth muscle in organophosphate-treated swine: 1. Agonist changes.

1. Male weanling swine were injected daily for up to 14 days with the organophosphate cholinesterase inhibitors, diisopropylfluorophosphate (DFP) or sarin. The clinical signs of poisoning disappeared or were attenuated by 7 days after starting the DFP treatment, indicating the development of tolerance to DFP toxicity. 2. A significant decrease in acetylcholinesterase activity (85-98%) occurred over the course of this treatment followed by a decrease in the maximal density (Bmax) of [3H] quinuclidinyl benzilate ([3H]QNB) and [3H] N-methylscopolamine ([3H]-NMS) binding sites in isolated cells. The affinity of the muscarinic receptors (KD) for [3H]QNB and [3H]NMS binding, however, remained unaffected. 3. Dose-response curves for ACh-induced increase in isometric tension of tracheal smooth muscle (TSM) showed a leftward shift from control, 2 h after DFP injection. Twenty-four hours after the last DFP treatment, for animals receiving 1 or up to 14 daily injections of DFP, all the dose-response curves were shifted to the left to approximately the same ACh sensitivity when compared with that for control tissue. 4. In vitro treatment of the muscle with 10(-4) M DFP shifted the dose-response curves leftward, in both control and injected animals, and rendered the muscles from control, 1- and 3-day injected animals sensitive to ACh concentrations as low as 10(-10) M. Sensitivity to 10(-10) M ACh was eliminated by carefully cleaning the smooth muscle of adherent connective tissue containing nerves and ganglia and after subacute treatment of swine for 7 days with DFP. DFP-induced spontaneous contractions were also eliminated by careful cleaning. 5. Subacute DFP treatment caused a small leftward shift in the dose-response curve for bethanechol at 2 h and a rightward shift at 1,3 and 7 days, compared to controls. 6. Dose-response curves for K+ were shifted to the right after 1 and 3 days of DFP treatment, but shifted back towards the control after 7 days of treatment. The muscle cells were hyperpolarized by approximately 5 mV after 7 days of DFP or sarin injections. The membrane potential was slightly more sensitive to changes in K+ concentration after 7 days of sarin injection. 7. Subacute treatment of swine with organophosphates modifies the response of neural elements in swine TSM to ACh. Chronic cholinesterase inhibition causes a reduction in the sensitivity of the neural elements to ACh. The decrease in muscarinic receptor density which occurs with chronic cholinesterase inhibition is not sufficient to explain tolerance to organophosphates since TSM maintains an almost normal responsiveness to ACh.

Acetylcholine↗
PubMed1990

Modulation of gastric acid secretion by peripheral presynaptic alpha 2-adrenoceptors at both sympathetic and parasympathetic pathways.

1. The effects of the alpha 2-adrenoceptor agonist detomidine, and the antagonists idazoxan and CH-38083 were examined on gastric acid secretion from non-vagotomized and vagotomized stomach lumen-perfused rats. The effects of detomidine on acid secretion from isolated guinea-pig gastric fundus were also evaluated. 2. In both non-vagotomized and vagotomized rats i.p. administration of detomidine significantly increased acid secretion, whereas i.c.v. detomidine was without effect. The stimulant action of i.p. detomidine was antagonized by both i.p. idazoxan and CH-38083 as well as by pretreatment with reserpine. 3. In vagotomized and reserpinized rats whose acid secretion was increased by electrical stimulation of the left vagus nerve, i.p. injection of detomidine caused inhibitory effects on acid secretion which were fully antagonized by both i.p. idazoxan and CH-38083. 4. Both idazoxan and CH-38083 caused a significant increase in acid secretion induced by vagal stimulation. At higher doses the two antagonists displayed a potentiating effect on vagally induced acid secretion only when they were associated to i.v. infusion of prazosin and propranolol. 5. Detomidine was without effect on acid secretion from isolated guinea-pig gastric fundus, whereas histamine or bethanechol caused a marked and dose-dependent stimulant action. 6. Overall, these results provide evidence that peripheral presynaptic alpha 2-adrenoceptors modulate both adrenergic inhibitory and cholinergic excitatory influences on rat gastric acid secretion.

Adrenergic alpha-Antagonists↗
PubMed1991

Is field (vagal) stimulation of gastric acid secretion mediated by M1 or non-M1 muscarinic receptors? A methodical problem exemplified in the mouse stomach in vitro.

1. Highly controversial claims have been put forward in the literature as to the involvement of either M1 or non-M1 muscarinic receptors in the field (vagal) stimulation of gastric acid secretion. This mini-review considers three available sets of data obtained in the mouse isolated, lumen-perfused stomach. 2. While pA2 values seemed to favour non-M1 receptors, a comparison between M1 selective versus non-selective antagonists on the one hand and field stimulation versus bethanechol stimulation on the other clearly pointed to M1 receptors being involved. 3. In the present review we discuss a novel experimental approach supporting the latter concept of M1 receptors. This novel approach provides a simple though provocative way to deal with the particular difficulties in determining pA2 values in the acid-secreting gastric mucosa. It is based on the rank order in the effects of different antagonists relative to their receptor type-dependent affinities, when employed at a fixed concentration, rather than on their pA2 values.

Animals↗
PubMed1972

Control of pancreatic amylase release in vitro: effects of ions, cyclic AMP, and colchicine.

1. The time course and concentration-response relationship of amylase release from pieces of guinea-pig pancreas in vitro in response to bethanechol and pancreozymin was determined.2. Removal of Ca(++) from the medium had no effect on basal amylase release but abolished the stimulating effect on release of bethanechol.3. Elevation of the concentration of Mg(++) in the medium increased basal amylase release and reduced the response to bethanechol.4. Elevation of the concentration of K(+) in the medium increased amylase release; this effect was blocked by a concentration of atropine which blocked also the response to bethanechol.5. Cyclic AMP, dibutyryl cyclic AMP and theophylline failed to stimulate amylase release. Pancreatic cyclic AMP concentrations were found not to be increased by bethanechol, pancreozymin or an elevated concentration of K(+) in the medium.6. Colchicine had no effect on basal amylase release or the response to bethanechol or pancreozymin.7. It is concluded that the coupling of stimulus to secretion involves ionic control but that neither cyclic AMP production nor microtubular mechanisms play a major role in controlling exocytosis in the pancreatic acinar cell. These findings are discussed in relation to the stimulus-secretion coupling processes in other cells.

Amylases↗
PubMed1976

Observations on the pharmacology of cholinoceptive neurones in the rat brain stem.

The pharmacology of spontaneously active cholinoceptive neurones in the brain stem of rats anaesthetized with urethane has been investigated using microiontophoresis to administer muscarinic and nicotinic agonists and antagonists. 2. Acetylcholine (ACh) excited most cells but occasionally depressed their activity. Muscarine, and the muscarinic agonists methacholine and bethanechol produced prolonged excitation or inhibition of cells whereas nicotine produced prolonged excitations but no inhibitions. 3 Atropine selectively antagonized ACh excitations and both excitation and inhibition of neuronal activity produced by muscarine and muscarinic agonists, but not the excitations produced by nicotine, glutamate or DL-homocysteic acid. 4 Dihydro-beta-erythroidine (DHBE) and tubocurarine antagonized both ACh and nicotine excitations but not those induced by glutamate or DL-homocysteic acid. Inhibitions by ACh or muscarine were not affected. 5 It is concluded that excitations of cholinoceptive neurones in the rat brain stem may be mediated by activation of both muscarinic and nicotinic receptors whereas inhibitions are mediated by activation of a muscarinic receptor.

Acetylcholine↗
PubMed1977

Comparative inhibitory effects of 3-quinuclidinyl benzilate (QNB) and atropine on amylase release from rat pancreas.

1 Secrection of amylase from rat pancreas stimualted by urecholine was studied in relation to its inhibition by atropine and 3-quinuclidinyl benzilate (QNB). 2 Urecholine-induced secretion was completely abolished by atropine at 10(-6)M and QNB at 10(-8)M. Significant inhibition could be detected at 10(-8)M atropine and 10(-10)M QNB. 3 The secretory response to pancreozymin was not blocked either by atropine or QNB. 4 The inhibitory effect of QNB remained for at least 90 min after its removal from the incubation medium. 5 It is concluded that QNB is 10 times more potent than atropine in inhibiting pancreatic amylase secretion induced by urecholine.

Amylases↗