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PubMed1980

Coronary vasoconstriction by locally administered acetylcholine, carbachol and bethanechol in isolated, donor-perfused, rat hearts.

1 Experiments were carried out on rat isolated heart preparations in which the coronary vasculature was perfused through the aorta at a constant flow rate with arterial blood from donor animals. Single doses of drugs were injected into the aortic cannula. 2 Small doses of acetylcholine, carbachol or bethanechol decreased perfusion pressure (PP) without markedly affecting left ventricular pressure (LVP) and heart rate (HR); larger doses of these drugs increased PP (vasoconstriction), and decreased LVP and HR in a dose-dependent manner. 3 Acetylcholine, carbachol and bethanechol had almost no effects when perfused through the aorta in such a way as to exclude the coronary vessels. 4 Coronary vasoconstriction in response to acetylcholine, carbachol and bethanechol was not significantly affected by reserpine pretreatment, phentolamine or hexamethonium, but was antagonized by small doses of atropine. 5 From these results it is concluded that in the coronary vasculature of the rat, the receptors involved in the vasoconstrictor actions of acetylcholine carbachol and bethanechol are muscarinic.

Acetylcholine↗
PubMed1981

Parallel maturation of the pancreatic secretory response to cholinergic stimulation and the muscarinic receptor population.

1 The appearance of pancreatic muscarinic receptors during development has been measured by use of the specific ligand [3H]-quinuclidinyl benzilate ([3H]-QNB). 2 QNB binding sites are present in foetal pancreas; their maximal concentration is attained at the age of 30 days and a significant decrease is observed in one year old animals. 3 Affinity of [3H]-QNB for the muscarinic receptor does not change with age. 4 An evaluation of the pancreatic secretory response to a cholinoceptor agonist as a function of age indicates that the development of this response parallels that of the receptor population. 5 It is suggested that, at all ages from 3 days after birth onwards, the maximal secretory response of the exocrine pancreas to a cholinoceptor agonist mobilizes the same proportion of the total population of QNB binding sites.

Aging↗
PubMed1982

Effects of H2-receptor antagonists and anticholinoceptor drugs on gastric and salivary secretion induced by bethanechol in the anaesthetized dog.

1 The H2-receptor antagonists, ranitidine and cimetidine, have been compared with atropine and pirenzepine for their effects on gastric acid output, and on salivary secretion from the left parotid gland in the anaesthetized dog. Gastric and salivary secretions were elicited by intravenous infusion of bethanechol. 2 Atropine (0.3-1 microgram/kg) or pirenzepine (3-10 micrograms/kg) reduced both gastric and salivary secretions, pirenzepine showing little evidence of any selectivity for gastric secretion. 3 The H2-receptor antagonists, ranitidine (30-1000 micrograms/kg) and cimetidine (100-3000 micrograms/kg), selectively inhibited gastric secretion and even at relatively high dose levels did not alter salivary volume.

Anesthesia↗
PubMed1982

Presynaptic muscarinic receptors inhibiting active acetylcholine release in the bullfrog sympathetic ganglion.

1 The effects of bethanechol and atropine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined electrophysiologically. 2 Bethanechol (1 mM) caused no depolarization of sympathetic preganglionic nerve terminals, whereas carbachol or ACh in the same concentration induced marked depolarizations of these terminals. 3 Bethanechol (10 microM) depressed the amplitude of fast excitatory postsynaptic potentials (e.p.s.ps) recorded in Ca2+-high Mg2+ solution, without depolarizing ganglion cells. The quantal content measured from these fast e.p.s.ps by the variance method showed a significant reduction. 4 Amplitudes of both miniature e.p.s.ps and ACh-potentials induced by iontophoresis of ACh were not affected by addition of bethanechol (10 microM). 5 The depressant effect of bethanechol (10 microM) on fast e.ps.ps disappeared in the presence of atropine (3 microM). 6 Atropine (3 microM) increased the quantal content measured from fast e.p.s.ps recorded in low Ca2+-high Mg2+ solution. 7 The depressant effect of bethanechol (10 microM) on fast e.p.s.ps was unaffected by alpha-adrenoceptor blocking agents (phenoxybenzamine (10 microM) or phentolamine (10 microM). 8 These results suggest that presynaptic nerve terminals in bullfrog sympathetic ganglia possess a muscarinic receptor which inhibits active release of ACh.

Acetylcholine↗
PubMed1983

The role of nicotinic receptors in dog pancreatic exocrine secretion.

1 The effects of pentamethonium, an autonomic ganglion blocker, were studied on the exocrine pancreatic secretion of six conscious dogs given intravenous infusions of urecholine, caerulein or pentagastrin on a background of submaximal doses of secretin. 2 Urecholine-induced protein secretion was not affected but both caerulein- and to a smaller extent, pentagastrin-induced protein secretions were depressed by pentamethonium. 3 These results indicate that intravenous caerulein and pentagastrin, but not urecholine, act at least partially via nicotinic receptors. 4 Volume and bicarbonate output were depressed by pentamethonium when stimulated by intravenous caerulein with a background of secretin, but not when stimulated by pentagastrin on a background of secretin. 5 From these data it is suggested that caerulein and pentagastrin may potentiate secretin-stimulated hydrelatic secretion by different mechanisms.

Animals↗
PubMed1983

Influence of dopamine receptor agonists on gastric acid secretion induced by intraventricular administration of thyrotropin-releasing hormone in the perfused stomach of anaesthetized rats.

1 The influence of dopamine receptor agonists on gastric acid secretion stimulated by thyrotropin-releasing hormone (TRH) was studied in the perfused stomach of anaesthetized rats. 2 Intraventricular TRH produced a dose-dependent stimulation of basal gastric acid secretion. 3 Pretreatment with apomorphine, bromocriptine or methamphetamine inhibited the TRH-stimulated gastric acid secretion; these drugs did not influence bethanechol-induced acid secretion. 4 Haloperidol and metoclopramide prevented the antisecretory effects of apomorphine, bromocriptine and methamphetamine. 5 The present study suggests that central dopamine receptor stimulation inhibits intraventricular TRH-induced gastric acid secretion in rats.

Anesthesia↗
PubMed1984

Relaxation of cat tracheobronchial and pulmonary arterial smooth muscle by vasoactive intestinal peptide: lack of influence by peptidase inhibitors.

Vasoactive intestinal peptide (VIP) caused concentration-dependent relaxation in precontracted segments of trachea, hilar bronchus, intrapulmonary bronchus and intrapulmonary artery (IPA) isolated from cat lungs. VIP-induced relaxation responses were abolished by preincubation of tissues with the proteolytic enzyme, alpha-chymotrypsin (2 units ml-1). At the concentration employed, alpha-chymotrypsin treatment did not adversely affect tissue viability as isoprenaline and bethanechol continued to relax airways and IPA, respectively. Aprotinin prevented enzymatic degradation of VIP by alpha-chymotrypsin as demonstrated by the ability of VIP to relax tissues incubated with both the peptidase inhibitor and alpha-chymotrypsin. A spectrum of peptidase inhibitors, including aprotinin, leupeptin, bestatin, bacitracin, beta-phenylpropionic acid and captopril, individually or in combination, did not augment the relaxant effects of VIP in isolated pulmonary tissues. These results suggest that local enzymatic degradation may not be a primary route for inactivation of VIP in cat isolated airways and IPA. If VIP acts as a neurotransmitter in these tissues, a mechanism other than enzymatic proteolysis may be responsible for terminating its action.

Airway Resistance↗
PubMed1987

Differential effects of pertussis toxin and lithium on muscarinic responses in the atria and ileum: evidence for receptor heterogeneity.

Pretreatment with pertussin toxin was shown to inhibit selectively muscarinic responses in the atria, but have no effect on responses in the ileum. The converse was true when the animals were pretreated with lithium. These data are consistent with the hypothesis that muscarinic receptors in the atria are coupled to an inhibition of adenylate cyclase, whilst those in the ileum are coupled to inositol phospholipid hydrolysis and indicate differences in the muscarinic receptors in these two tissues.

Adenylate Cyclase Toxin↗
PubMed1987

Muscarinic agonists block five different potassium conductances in guinea-pig sympathetic neurones.

Muscarinic excitation of sympathetic ganglion cells has usually been thought to result from inhibition of an outward K+ current, the M current, although in other neurones several conductances have been shown to be blocked by muscarinic agonists. We report that, as well as resting K+ conductance, all of four different K+ conductances, two voltage-dependent (M currents and A currents) and two calcium-dependent (responsible for slow and very slow afterhyperpolarizations), present in different sub-types of guinea-pig sympathetic neurones, are inhibited by the muscarinic agonists, bethanechol and muscarine. All of these effects increase neurone excitability and can lead to repetitive discharge.

Action Potentials↗
PubMed1987

Contractile effects of substance P and neurokinin A on the rat stomach in vivo and in vitro.

Substance P and neurokinin A (substance K) were infused into the coeliac artery of anaesthetized rats at doses of 0.06-20 nmol min-1. Both tachykinins caused contractions of the stomach, the threshold dose of neurokinin A being 10 times lower than of substance P. The dose-response curve for substance P was flatter than that for neurokinin A. On circular muscle strips from the rat gastric corpus in vitro, the dose-response curves for both tachykinins were parallel, neurokinin A being 10 times more potent than substance P. The contractions in response to 10 microM neurokinin A and to 30 microM substance P were 58 and 54%, respectively, of the maximal contraction to bethanechol (1 mM). The effect of substance P was reduced by atropine both in vivo and in vitro. In vitro, the contractions to substance P were also reduced by tetrodotoxin but left unaffected by methysergide. The action of neurokinin A was not affected by these drugs. It is concluded that neurokinin A contracts rat stomach by a direct action on the circular smooth muscle, whereas the action of substance P is mediated, at least in part, by cholinergic interneurones.

Animals↗
PubMed1988

Quantitative effects of some muscarinic agonists on evoked surface-negative field potentials recorded from the guinea-pig olfactory cortex slice.

1. The effects of muscarinic receptor agonists on the electrically-evoked surface-negative field potential (N-wave) were measured in the guinea-pig olfactory cortex slice maintained in vitro. 2. Bath-superfusion of (+/-)-muscarine, acetylcholine (ACh), carbachol (CCh), or methacholine (MCh) (10-200 microM) produced reversible, dose-dependent depressions of the N-wave (ACh and MCh effects were observed in the presence of 10 microM neostigmine). The order of potencies (based on agonist dose causing 50% field depression: IC50) was: ACh greater than or equal to muscarine greater than CCh greater than MCh. All four agonists depressed the field potential by 100% at doses greater than 500 microM. 3. Pilocarpine and bethanechol were weak agonists and only produced measurable effects at high doses (1-2 mM). Neither agonist evoked a maximum response at doses up to 10 mM. 4. The muscarinic ganglion stimulant, McN-A-343 yielded inconsistent results, depressing the field potential in some slices, but having no effect in others. Pre-application of a conditioning dose (100 microM) of McN-A-343 reduced subsequent responses to CCh, suggesting possible partial agonist properties. 5. Oxotremorine (up to 100 microM) did not depress the field potential, but it reversibly antagonized the effects of CCh. 6. It is concluded that reproducible, quantifiable responses to muscarinic agonists can be evoked in the olfactory cortex slice. We suggest this preparation may be useful for conducting pharmacological studies of 'intact' central muscarinic receptors.

Acetylcholine↗
PubMed1991

Modulation of gastric contractions in response to tachykinins and bethanechol by extrinsic nerves.

1. Extrinsic reflexes elicited by changes in gastric wall tension play an important role in regulating gastric tone. The present study investigated whether such reflexes modulate gastric contractions induced by close arterially administered neurokinin A (NKA), substance P (SP), SP-methylester and bethancehol in anaesthetized rats. 2. Reflex pathways were acutely interrupted by either subdiaphragmatic vagotomy or prevertebral ganglionectomy. C-fibre afferent nerve activity was abolished by pretreating rats with capsaicin 10 to 16 days before the experiments. 3. The order of potency in inducing gastric contractions was NKA greater than SP greater than bethanechol. SP-methylester was markedly less effective than SP and its effects did not fit sigmoid dose-response curves (DRCs). The maximal responses to NKA, SP, and bethanechol were similar, whilst the DRC for SP was significantly flatter than those for NKA or bethanechol. Pretreatment of the rats with the peptidase inhibitors phosphoramidon or captopril did not increase the contractile response to SP. 4. Prevertebral ganglionectomy had no significant effect on the DRCs for SP and NKA, whereas vagotomy shifted the DRCs for all three test substances to the left. 5. Capsaicin pretreatment did not change the DRC for NKA in rats with intact vagus but shifted that for bethanechol to the left. The leftward of the DRC for NKA caused by vagotomy was prevented in capsaicin-pretreated rats whereas the vagotomy-induced shift of the DRC for bethanechol remained unaltered. The shift of the DRC for SP seen in response to vagotomy was only slightly reduced by capsaicin pretreatment. 6. These data may be interpreted as demonstrating two neuronal mechanisms for modulating drug-induced gastric contractions. First, the contractions themselves activate a vago-vagal negative feedback involving capsaicin-sensitive afferents. Second, NKA, and to a lesser degree SP, seem to induce a nonvagal non-splanchnic mechanism which via capsaicin-sensitive afferent neurones reinforces tachykinininduced gastric contractions.

Animals↗
PubMed1991

The effect of CCKB/gastrin antagonists on stimulated gastric acid secretion in the anaesthetized rat.

1. The urethane-anaesthetized, vagotomised rat preparation was used to investigate the effects of the histamine H2-antagonist ranitidine, the proton pump inhibitor omeprazole and the CCKB/gastrin antagonists CI-988, PD 136450 and L-365,260 on pentagastrin-, histamine- and bethanechol-induced gastric acid secretion. 2. The novel CCKB/gastrin antagonists CI-988 and PD 136450, and L-365,260 dose-dependently inhibited pentagastrin-induced secretion. The ED50 value for PD 136450 was 0.05 mumol kg-1, the same following intravenous or subcutaneous administration. 3. CI-988 and PD 136450 administered subcutaneously at dose levels highly effective for antagonism of pentagastrin responses had no effect on basal acid secretion. 4. Ranitidine inhibited pentagastrin-, bethanechol-, and histamine-induced acid secretion, whereas the CCKB/gastrin antagonists inhibited only the secretory response to pentagastrin. 5. The selective CCKA antagonist, devazepide, was inactive at up to 300 mumol kg-1 i.p. against the three stimulants of acid secretion. 6. CI-988 and PD 136450 will be useful research tools with which to investigate the role of CCKB/gastrin receptors in gastric acid secretion and the trophic activities of gastrin and cholecystokinin (CCK) on the gastrointestinal tract.

Animals↗
PubMed1992

Characterization of muscarinic receptors that mediate contraction of guinea-pig isolated trachea to choline esters: effect of removing epithelium.

1. The muscarinic receptor subtype that mediates contraction of guinea-pig trachea, in the presence and absence of epithelium, to acetic and carbamic acid choline esters was determined by use of preferential muscarinic receptor antagonists: pirenzepine (M1 receptor), methoctramine (M2 receptor) and 4-diphenylacetoxy-N-methylpiperidine (4-DAMP) (M3 receptor). 2. Acetylcholine (ACh), methacholine (MeCh), carbachol (CCh), bethanechol (BeCh) and oxotremorine induced concentration-dependent contraction of guinea-pig isolated tracheal strips in the presence and absence of epithelium. Contraction to acetic choline esters (ACh and MeCh) was augmented by removal of the epithelium, whereas contraction to carbamic acid choline esters (CCh and BeCh) and oxotremorine was not influenced by removal of the epithelium. 3. Pirenzepine, methoctramine and 4-DAMP caused parallel rightward displacements of the concentration-contraction curves to the muscarinic agonists. The pA2 values (determined from Arunlakshana-Schild graphs) for pirenzepine and 4-DAMP in guinea-pig trachea in the presence of epithelium were: ACh as the agonist, 7.6 and 9.0, respectively; CCh as the agonist, 7.6 and 9.1, respectively. The apparent pKB values for methoctramine with the same system were: ACh as the agonist, 5.6; CCh as the agonist, 5.6. Similar values were obtained with MeCh, BeCh and oxotremorine as the agonists. These values were agonist- and epithelium-independent. 4. It is concluded from the pA2 and apparent pKB values obtained for the muscarinic receptor antagonists used in this study that contraction of guinea-pig isolated trachea, with and without epithelium, to both acetic and carbamic acid choline esters is mediated via the muscarinic M3 receptor subtype.Differential contractile responses of guinea-pig trachea to acetic and carbamic acid choline esters upon the mechanical removal of the epithelium may not be explained by activation of different muscarinic receptor subtypes by these agonists.

Acetylcholine↗
PubMed1993

Effects of the immunosuppressants cyclosporin A and FK 506 on exocytosis in the rat exocrine pancreas in vitro.

1. We have examined the effects of the immunosuppressive drugs cyclosporin A (CsA) and FK 506 on exocytosis in two in vitro preparations of the exocrine pancreas-lobules and dispersed acini. 2. In lobules taken from starved rats and stimulated with the secretagogue caerulein, both CsA and FK 506, given shortly before stimulation, caused a dose-dependent inhibition of amylase secretion. In lobules from rats that had been pretreated in vivo with the protease inhibitor FOY-305 to stimulate secretion maximally, both CsA and FK 506 inhibited secretion of newly synthesized proteins, whereas only FK 506 inhibited caerulein-stimulated amylase release. 3. These different effects of the immunosuppressants on amylase release were reflected in their effects on degranulation, as revealed by electron microscopy. Control acinar cells in lobules from FOY-305-treated rats were almost completely degranulated, whereas treatment with FK 506, but not CsA, caused the accumulation of zymogen granules close to the apical plasma membrane. 4. In dispersed acini, stimulated with the cholinomimetic secretagogue bethanechol, both CsA and FK 506 reduced the secretory response, to about 45% of control; IC50 values were 50 nM and 3 nM, respectively. A similar partial inhibition of exocytosis was seen in acini permeabilized with the bacterial toxin streptolysin O and stimulated with 10 microM Ca2+. 5. These results demonstrate that the immunosuppressants cause an inhibition of exocytosis in the exocrine pancreas that is both rapid in onset and potent. The loss of the inhibitory effect of CsA on amylase release in lobules taken from FOY-305-treated rats may reveal a change in the characteristics of exocytosis as a consequence of the high level of stimulation, and also indicates that CsA and FK 506 have subtly different effects on secretion. We suggest that these drugs might be useful tools in the dissection of the molecular mechanisms of exocytosis.

Amylases↗
PubMed1994

Differential effects of Na+, K(+)-ATPase inhibition by ouabain on acid secretory responses to histamine and bethanechol in the mouse isolated stomach.

1. The effect of Na+,K(+)-ATPase inhibition by ouabain on gastric acid secretion was studied in the mouse isolated whole stomach preparation. 2. Ouabain caused a transient enhancement of histamine-induced gastric acid secretion followed by an inhibitory phase. On the other hand, ouabain caused a rapid reduction of bethanechol-stimulated acid secretion without an enhancement phase. 3. In dibutyryl cyclic AMP-induced acid secretion, ouabain led to a transient increase in acid secretion followed by a fall, as was seen with the histamine stimulation. Ouabain caused a rapid reduction of A23187-induced acid secretion. 4. Ouabain by itself increased basal acid secretion, and thereafter slowly suppressed the acid secretion. 5. Atropine inhibited both the ouabain-induced enhancement of the stimulated gastric acid secretion and the ouabain-induced stimulation of basal acid secretion. 6. The present study showed that Na+,K(+)-ATPase inhibition by ouabain caused a phasic enhancement of the stimulated gastric acid secretion through release of endogenous acetylcholine when the secretagogues act via an intracellular cyclic AMP pathway. It also inhibited the stimulated acid secretion irrespective of secretagogues, probably through its inhibitory effect on Na+,K(+)-ATPase in the gastric parietal cell.

Animals↗
PubMed1978

Adrenergic innervation and adrenergic mechanisms. A study of the human urethra.

Adrenergic nerves studied by a histochemical method were uniformly distributed along the whole extent of the male and female urethra. Corresponding to the adrenergic innervation a preponderance of contraction-mediating alpha-adrenoceptors was found in vitro studying urethral strips and in vivo recording the urethral closure pressure profile (UCPP). Norephedrine significantly reduced incontinence and increased UCPP in stress-incontinent women.

Adrenergic Fibers↗
PubMed1975

Effect of bulbar acidification on gastric acid responses to urecholine in Pavlov pouch dogs.

Dogs were provided with mucosal septal pouches of the fundic stomach and of the duodenal bulb. Gastric secretion was stimulated by intravenous infusion of submaximal doses of porcine gastrin or the stable choline ester Urecholine. Acid perfusion of bulbar pouches profoundly inhibited acid responses to gastrin. Bulbar acidification produced little or no reduction in acid secretion induced by Urecholine. Small doses of Urecholine do not release gastrin in the dog but may induce acid secretion, mainly by direct cholinergic stimulation of the HCl glands. The fact that Urecholine-induced acid secretion was not inhibited in the present experiments is consistent with the hypothesis that the bulbar mechanism does not interfere with cholinergic stimulation acting on the parietal cells.

Animals↗