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PubMed1984

The time course of muscarinic depolarization of guinea-pig myenteric neurones.

Intracellular recordings were made from neurones in the myenteric plexus of the guinea-pig ileum in vitro. Muscarinic depolarizations were evoked by brief (1-500 ms) ionophoretic applications of acetylcholine (ACh) or other agonists. Nicotinic responses to ACh evoked by the same ionophoretic pulse had short latencies and rapid rise times, indicating close proximity of the ionophoretic pipette to the neurone membrane. The time course (duration several seconds) of the muscarinic depolarization was independent of the identity of the agonists applied (ACh, methacholine, carbachol, oxotremorine). Hyoscine and barium were ejected onto the neurones by brief (30 ms-1 s) pressure pulses applied to micropipettes. Hyoscine applied immediately after ACh, during the latency and rising phase of the muscarinic depolarization, did not antagonize the response to ACh. The same application of hyoscine immediately prior to ACh caused complete antagonism. Muscarinic depolarizations evoked by continuous application of ACh (by repeated ionophoresis or perfusion) were reversed by hyoscine. The time course of this reversal was similar to the decline of the muscarinic response following a single brief application of ACh. Barium caused a depolarization similar to that produced by muscarinic agonists in its latency, time course and temperature sensitivity, and having the same reversal potential (-90 mV). These barium potentials were not affected by hyoscine. It is suggested that neither diffusion of ACh to the receptors nor the kinetics of the agonist-receptor interaction contributes significantly to the latency and prolonged time course of the muscarinic depolarization.

Acetylcholine↗

PubMed1984

Release of kallikrein-like esterase and tonin from dispersed cells of the rat submandibular gland.

Viable dispersed cell preparations of rat submandibular gland were obtained by a tissue-dissociation procedure using collagenase and gentle mechanical force. The cells released kallikrein-like esterase in a time- and calcium-dependent manner in response to noradrenaline (10 microM) at 30 degrees C. The net loss of kallikrein-like esterase content from the dispersed cells corresponded with the increase in kallikrein-like esterase activity in the suspending medium at all concentrations of noradrenaline. These results indicate the viability and functional integrity of this dispersed cell preparation of rat submandibular gland. alpha-Adrenoceptor agonists such as noradrenaline stimulated kallikrein-like esterase and tonin release in a dose-dependent manner, whereas the beta-adrenoceptor agonist isoprenaline and cholinoceptor agonist methacoline were both inactive. Noradrenaline-induced release of kallikrein-like esterase and tonin were completely blocked by prior addition of the alpha-adrenoceptor antagonist, phenoxybenzamine. It is concluded that the secretion of kallikrein-like esterase and tonin in rat submandibular gland is mediated only via stimulation of alpha-adrenoceptors.

Adrenergic alpha-Agonists↗

PubMed1984

The calcium dependency of mucus glycoconjugate secretion by canine tracheal explants.

Canine tracheal explants, incubated overnight with [14C]-glucosamine, elicited an enhanced secretion of ethanol-precipitated 14C-labelled glycoconjugate when challenged with methacholine, 10 microM. Explants were rendered deficient in total calcium content and unresponsive to methacholine, 10 microM, by incubating them in calcium-free medium for 18 to 22 h; however, the secretory response to the cholinergic agonist was restored with the addition of calcium to the medium. A dose-response relationship resulted when explants were challenged with methacholine in nutrient medium containing varied calcium concentrations (0.45 to 7.2 mM); alterations in the calcium concentration in the absence of methacholine had no significant effect on the basal secretion of 14C-labelled glycoconjugate. The calcium-selective ionophore A23187, 10 microM, stimulated [14C]-glycoconjugate secretion and induced the most significant effect in the presence of nutrient medium containing calcium. Verapamil, 10 microM, a calcium-entry blocker failed to inhibit basal or stimulated [14C]-glycoconjugate secretion; however, the intracellular calcium antagonist TMB-8, 10 to 100 microM, inhibited methacholine-induced [14C]-glycoconjugate secretion in a dose-dependent manner. These data suggest that respiratory mucus secretion is a calcium-dependent process and that intracellular calcium is more vital than extracellular calcium in supporting this phenomenon.

Animals↗

PubMed1985

Comparison of the action of cholinomimetics and pentagastrin on gastric secretion in dogs.

Stimulation of acid secretion by muscarinic cholinomimetic agents depended on the periodic interdigestive activity of the stomach. This explains the peak and following fade. Pentagastrin stimulated gastric secretion after a fixed interval and did not depend on the interdigestive activity. Neither gastrin nor methacholine directly contracted the gallbladder in the doses used. A sustained secretion of gastric acid and pepsin, such as follows a meal, required both hormonal stimulation and gastric distension. The magnitude of the acid response from Heidenhain pouches following meals suggested that pentagastrin doses commonly used experimentally greatly exceed the physiological.

Animals↗

PubMed1985

Affinity and efficacy of racemic, (+)-, and (-)-methacholine in muscarinic inhibition of [3H]-noradrenaline release.

The right postganglionic sympathetic nerves of rat isolated perfused hearts (previously loaded with [3H]-noradrenaline) were stimulated electrically with 10 trains of 10 pulses at 10 Hz. The inhibition by methacholine of stimulation-evoked [3H]-noradrenaline overflow into the perfusate (determined in the presence of corticosterone, desipramine, phentolamine, and propranolol) was taken as a measure for activation of presynaptic muscarinic receptors. The evoked [3H]-noradrenaline overflow was inhibited by (+)-, racemic, and (-)-methacholine in a reversible and concentration-dependent manner. The concentration causing 50% inhibition (IC50) was 0.1, 0.26, and 65 microM, respectively, resulting in an isomeric potency ratio IC50 (+)/IC50(-) of 650. The dissociation constant KA of the (+/-)- or (+)-methacholine-presynaptic receptor complex was determined after fractional receptor inactivation according to Furchgott & Bursztyn (1967) with phenoxybenzamine or propylbenzilylcholine mustard as irreversible antagonists of muscarinic receptors. KA for (-)-methacholine was estimated according to Mackay (1966). KA of (+)-, (+/-)-, and (-)-methacholine were 2.5, 4 and 440 microM, resulting in an isomeric affinity ratio KA (+)/KA(-) of 180. The discrepancy between the isomeric IC50 ratio and the isomeric KA ratio is explained by a higher intrinsic efficacy of the (+)-enantiomer compared to the (-)-enantiomer. Thus, (+)-methacholine has to occupy fewer receptors to induce a given inhibition of release than its antipode as revealed by a plot of fractional receptor occupancy vs response. The results show that, in the effector system of presynaptic muscarinic inhibition, methacholine enantiomers differ greatly not only in affinity for the receptor, but also to some extent in the efficiency of signal transmission, and both parameters contribute to the high isomeric potency ratio. The activity of the racemate is fully accounted for by the activity of the (+)-enantiomer.

Animals↗

PubMed1986

Comparison of the parasympatholytic activity of ACC-9358 and disopyramide.

ACC-9358 (N-[(3,5-di(pyrrolidinylmethyl)-4-hydroxy)benzoyl]aniline) is a newly developed analogue of changrolin, an antiarrhythmic agent used in the Peoples Republic of China. Since changrolin and other antiarrhythmic agents exert parasympatholytic activity which may limit their clinical usefulness, it was of interest to examine the parasympatholytic effects of ACC-9358. For comparative purposes we also studied the parasympatholytic activity of disopyramide. In guinea-pig isolated ileal strips, disopyramide, 3-30 microM, and ACC-9358, 100-300 microM, competitively antagonized carbachol-induced contractions with pA2 values of 5.78 and 4.17, respectively. In guinea-pig isolated right atria, disopyramide 3-30 microM, competitively antagonized methacholine-induced slowing of spontaneous beating with a pA2 value of 5.99 whereas ACC-9358, 3-300 microM, produced no significant muscarinic blockade in this preparation. Disopyramide (1.9-15 mg kg-1, i.v.), but not ACC-9358 (7.5-1.5 mg kg-1, i.v.), significantly increased rat pupil diameter in vivo. Disopyramide and ACC-9358 blocked vagal-induced reductions in heart rate in dogs anaesthetized with pentobarbitone. ED50 values were approximately 0.65 and 11.25 mg kg-1, respectively. We conclude that ACC-9358 possesses significantly less parasympatholytic activity than disopyramide.

Animals↗

PubMed1986

Alpha 2-adrenergic hyperpolarization is not involved in slow synaptic inhibition in amphibian sympathetic ganglia.

The adrenaline-induced hyperpolarization (AdH), slow inhibitory postsynaptic potential (slow i.p.s.p.) and hyperpolarizing phase of the response to methacholine (MChH) in Rana pipiens sympathetic ganglia were studied by means of the sucrose-gap technique. Desmethylimipramine (DMI, 0.5 microM) lowered the EC50 for adrenaline from 1.65 microM (1.23-2.21 microM, n = 10) to 0.30 microM (0.21-0.41 microM, n = 8). DMI did not potentiate the slow i.p.s.p. or the MChH. Propranolol, sotalol or prazosin (1 microM) did not antagonize the AdH. The response was antagonised by phentolamine (IC50 = 0.53 microM), yohimbine (IC50 = 6.2 nM) and idazoxan (IC50 = 0.59 microM). Yohimbine (0.1 microM) did not reduce the amplitude of the slow i.p.s.p. or the MChH. The slow i.p.s.p. was eliminated in Ringer solution containing Cd2+ (100 microM). This concentration of Cd2+ did not reduce the amplitude of the MChH. Alpha-Methylnoradrenaline produced a concentration-dependent hyperpolarization with an EC50 of 0.31 microM (0.13-0.73 microM, n = 5), in the presence of DMI (0.5 microM). These results are consistent with the hypothesis that the AdH may be generated by activation of a receptor similar to the mammalian alpha 2-adrenoceptor. No evidence was found in support of the hypothesis that an adrenergic interneurone is involved in the synaptic pathway for the slow i.p.s.p.

Adrenergic alpha-Agonists↗

PubMed1986

Dissociation constants and relative efficacies of acetylcholine, (+)- and (-)-methacholine at muscarinic receptors in the guinea-pig ileum.

Dissociation constants (KA) and relative efficacies of acetylcholine, (+)-methacholine and (-)-methacholine at muscarinic receptors in the guinea-pig isolated ileum were determined in the absence and presence of the cholinesterase inhibitor diisopropylfluorophosphate. The method used involved analysis of dose-response data before and after fractional inactivation of receptors with propylbenzilylcholine mustard. The KA values, estimated after cholinesterase inhibition, of acetylcholine, (+)- and (-)-methacholine were 1.7, 2.0 and 620 microM, respectively. The large (730 fold) difference in spasmogenic activity between (+)- and (-)-methacholine is due primarily to a difference in affinity for ileal muscarinic receptors although differences in efficacy (2 to 4 fold) also contribute. It is suggested that the methyl group at the chiral centre of (+)-methacholine has no apparent effect on the binding to muscarinic receptors, whereas the corresponding methyl group of (-)-methacholine interferes with binding, presumably by stabilizing a conformation of the drug which does not fit the receptor very well.

Acetylcholine↗

PubMed1986

Muscarinic receptor modulation of release of [Met5]enkephalin immunoreactive material and catecholamines from the bovine adrenal gland.

Muscarinic receptor modulation of secretion from the adrenal medulla was studied using retrogradely perfused bovine tissue. Atropine, at a dose not affecting 1,1 dimethyl-4-phenylpiperizinium (DMPP)-stimulated release, inhibited the acetylcholine (ACh)-stimulated release of noradrenaline and [Met5]enkephalin-immunoreactive material (ME-IRM). DMPP-stimulated release of catecholamines and ME-IRM was potentiated by the addition of methacholine. Pilocarpine significantly potentiated the release of noradrenaline only. Methacholine, pilocarpine or muscarine, when infused alone, had no stimulatory affect on the basal release of ME-IRM. These findings suggest that the muscarinic receptors in the bovine adrenal medulla function by potentiating the release of ME-IRM and catecholamines induced by nicotinic receptor stimulation.

Acetylcholine↗

PubMed1987

The effect of vasoactive intestinal peptide on smooth muscle tone and mucus secretion from the ferret trachea.

The effect of vasoactive intestinal peptide (VIP) was examined on the smooth muscle contraction and mucus secretion produced by methacholine and phenylephrine in the ferret whole trachea in vitro. VIP (0.5 to 800 nM) produced a concentration-dependent relaxation of the ferret trachea contracted by methacholine (1 microM) and phenylephrine (10 microM). The concentration-response curves for methacholine- and phenylephrine-induced contractions were both shifted to the right by VIP (0.1 microM). Methacholine-induced secretion was inhibited in a concentration-dependent manner by VIP, whereas that due to phenylephrine was enhanced. The concentration-response curve for methacholine-induced secretion was shifted to the right by VIP, whereas the curve for phenylephrine was shifted to the left. Methacholine produced a concentration-dependent increase in the rate of output of lysozyme from the ferret trachea with no corresponding increase in the concentration of lysozyme in the mucus. Phenylephrine produced a concentration-dependent increase in the rate of output and in the concentration of lysozyme. VIP (0.1 microM) significantly increased the concentration of lysozyme in the mucus produced by methacholine with no increase in the rate of lysozyme output. However, the rate of lysozyme output due to phenylephrine was significantly increased by VIP (0.1 microM) with no increase in concentration. We suggest that VIP inhibits secretion from mucous cells stimulated by methacholine, and enhances the secretion produced by phenylephrine from serous cells.

Animals↗

PubMed1988

Subtypes of muscarinic receptor on cholinergic nerves and atrial cells of chicken and guinea-pig hearts.

1. Electrically driven chicken and guinea-pig atria were used to investigate the negative inotropic effects of the muscarinic agonists methacholine and acetylcholine (ACh). The release of ACh from isolated hearts into the perfusate in response to (preganglionic) vagal or (pre- and postganglionic) field stimulation was bioassayed on the guinea-pig ileum or determined by labelling with [3H]-choline. 2. Concentration-response curves for the negative inotropic effect of methacholine were shifted to the right by pirenzepine in various concentrations (0.03 to 10 mumol l-1). The pA2 values were 7.76 in chicken atria and 6.53 in guinea-pig atria. Pirenzepine and atropine antagonized the negative inotropic response to 0.3 mumol l-1 ACh. The half-maximally effective concentrations (IC50) of pirenzepine (Pz) and atropine were 40 and 5.4 nmol l-1 in chicken atria and 330 and 3.5 nmol l-1, respectively, in guinea-pig atria. Thus, the respective potency ratios (IC50Pz/IC50atropine) were 7.4 and 94.3 in the two species. 3. Pirenzepine in low concentrations increased the release of unlabelled and 3H-labelled ACh from isolated hearts evoked by vagal and field stimulation only in chicken, but not in guinea-pigs. The half-maximally-effective concentration of pirenzepine was about 30 nmol l-1 in the chicken heart, whereas, in the guinea-pig heart, an increased release was observed at 300 nmol l-1. 4. (+)-Tubocurarine [(+)-Tc; 100 mumol l-1] reduced the release of ACh evoked by (preganglionic) vagal stimulation to a (+)-Tc-resistant release of about 30%. The time-course of the neuronal release of [3H]-ACh was markedly altered: the onset was delayed and the termination was extended beyond the period of stimulation (1 min or 5s) by several seconds. The (+)-Tc-resistant release was nearly abolished by 30 nmol l-1 pirenzepine. 5. In conclusion, the pre- and post-synaptic muscarinic receptors of the parasympathetic neuroeffector junction of the heart both belong to the M1-subtype in the chicken and to an M2-subtype in the guinea-pig. Block of the nicotinic ganglionic transmission in the chicken heart by (+)-Tc unmasked a muscarinic transmission, which presumably was mediated through M1-receptors stimulating a low and prolonged postganglionic release of ACh.

Acetylcholine↗

PubMed1988

Comparison of mucus flow rate, radiolabelled glycoprotein output and smooth muscle contraction in the ferret trachea in vitro.

1. The concentration-response curves for rate of mucus output, labelled-glycoprotein output and smooth muscle contraction in response to methacholine, phenylephrine and salbutamol were determined in the ferret trachea in vitro. 2. The potencies of methacholine and phenylephrine are both in order: smooth muscle contraction, glycoprotein output, rate of mucus output. 3. At lower concentrations methacholine is more potent than is phenylephrine on smooth muscle contraction, glycoprotein output and rate of mucus output. 4. Concentration-response curves for salbutamol show very little change in rate of mucus output but a large increase in glycoprotein output. 5. It is concluded that the glycoprotein output induced by salbutamol may come from a source different from those induced by methacholine and phenylephrine.

Albuterol↗

PubMed1988

Tachykinin involvement in parasympathetic nerve-evoked salivation of the ferret.

1. The tachykinin antagonist (D-Arg1, D-Cl2Phe5, Asn6, D-Trp7.9, Nle11)-substance P, injected intravenously, blocked salivary secretion from the ferret parotid and submandibular glands in response to subsequent i.v. injections of the tachykinins, substance P and neurokinin A. 2. The tachykinin antagonist reduced the parasympathetic nerve-evoked secretion of parotid and submandibular saliva by 15-20% and 35-40%, respectively. Atropine abolished the remaining secretory response. 3. The 'atropine-resistant' parasympathetic nerve-evoked secretion of saliva from the parotid and submandibular glands (about 5 and 30%, respectively, of that before administration of atropine) was abolished by the tachykinin antagonist. 4. The tachykinin antagonist was without effect on the protein concentration of parotid and submandibular saliva secreted in response to parasympathetic nerve stimulation. Parotid and submandibular saliva lacked amylase. 5. Atropine reduced the protein concentration of the submandibular saliva secreted in response to parasympathetic nerve stimulation by 50%; this was the protein concentration of substance P-evoked saliva. 6. The secretory response to methacholine and to stimulation of preganglionic sympathetic nerve fibres, tested in rats, was unaffected by the tachykinin antagonist, contra-indicating an unspecific action of the antagonist. 7. The results suggest that the neuronal release of tachykinins is probably important in the nerve-evoked secretory response of the parotid and submandibular glands.

Amylases↗

PubMed1988

Effects of leukotriene D4 on the mechanical and electrical properties of guinea-pig isolated trachealis.

1. The effects of leukotriene D4 (LTD4) on mechanical and electrical activity were examined in guinea-pig isolated trachealis muscle and compared with two other bronchoconstrictors, methacholine and potassium chloride (KCl). 2. LTD4 elicited concentration-dependent increases in tension in trachealis muscle which were slower in time course than responses induced by either methacholine or KCl. The maximum response to LTD4 was approximately 85% of the methacholine maximum. 3. At a concentration close to the EC50 for tension changes, LTD4 had no significant effect on either transmembrane potential or slow wave activity recorded in single trachealis cells. 4. At a concentration close to the EC90 for tension changes, LTD4 caused significant membrane depolarization, transiently reduced the amplitude and increased the frequency of slow wave discharge and ultimately abolished slow wave discharge. LTD4-induced depolarization was less marked, and developed more slowly, than that evoked by either methacholine or KCl. 5. These results show that LTD4 can elicit substantial increases in tension without altering transmembrane potential and are consistent with the view that LTD4 initiates contraction mainly through potential-independent mechanisms. However, at high concentrations the depolarization evoked by LTD4 allows the possibility that potential-dependent mechanisms may contribute to the spasm.

Airway Resistance↗

PubMed1988

Effects of anterior hypothalamic lesions and sham-operations on bacterial endotoxin-induced non-specific airway hyperreactivity in vivo and in vitro.

1. In the present study the effects of anterior hypothalamic (AHA) lesions and sham-operations were investigated on the endotoxin-induced airway hyperreactivity in guinea-pigs. Unoperated, sham-operated and AHA-lesioned guinea-pigs were injected intraperitoneally with Escherichia coli endotoxin and the airway reactivity tested four days later in isolated tracheal spirals and in spontaneously breathing anaesthetized animals. Control animals were given sterile saline. 2. Sham-operated control animals demonstrated a diminished responsiveness of the tracheal spirals in vitro and of the lung resistance (delta R1) in vivo to histamine receptor and cholinoceptor-muscarinic agonists as compared to unoperated control animals. 3. AHA-lesioned control animals showed a responsiveness of the respiratory airways in vitro and in vivo between the values of unoperated and sham-operated control animals, suggesting that lesions partially restored the diminished responsiveness. 4. In unoperated and sham-operated guinea-pigs, endotoxin administration induced hyperreactivity of the tracheal spirals and delta R1 to histamine receptor and cholinoceptor-muscarinic agonists with respect to the control groups. 5. In AHA-lesioned animals, the endotoxin-induced airway hyperreactivity in vitro and in vivo to histamine receptor and cholinoceptor-muscarinic agonists was absent.

Airway Resistance↗

PubMed1988

Purine receptors and guinea-pig trachea: evidence for a direct action of ATP.

1. Adenosine (3-300 microM) and ATP (1-300 microM) each induced concentration-dependent relaxation of guinea-pig isolated tracheal preparations that had been precontracted with methacholine. 2. Ectonucleotidase enzymes on the trachea dephosphorylated ATP to form adenosine which was then further metabolised to inosine and hypoxanthine. 3. Dipyridamole (2 microM) inhibited the metabolism of adenosine but did not inhibit the dephosphorylation of ATP. Nevertheless dipyridamole potentiated the effects of both adenosine and ATP in relaxing tracheal smooth muscle. 4. Although adenosine 5'-[beta,gamma-imido] triphosphate (AMP-PNP), an analogue of ATP, was resistant to catabolism by ectonucleotidases, it was more potent at inducing relaxation than either ATP or adenosine, and was also potentiated by dipyridamole (2 microM). 5. Relaxations induced by ATP and by AMP-PNP were more rapid than those induced by adenosine. 6. We therefore conclude that the intact ATP molecule can itself induce relaxation of the guinea-pig trachea, without first having to be metabolised to adenosine, and furthermore that dipyridamole does not act simply by inhibiting the degradation (or uptake) of adenosine.

Adenosine↗

PubMed1988

The effects of peptide histidine isoleucine and neuropeptide Y on mucus volume output from the ferret trachea.

1. The effects of peptide histidine isoleucine (PHI) and neuropeptide Y (NPY) were examined on the mucus volume output produced by methacholine and phenylephrine in the ferret whole trachea in vitro. 2. Sustained application of methacholine (5 microM) or phenylephrine (20 microM) produced a maintained volume output of mucus from the trachea. Both these agonists also increased the output of lysozyme (a marker for serous cell secretion). 3. PHI inhibited the maintained mucus volume output produced by methacholine but had no effect on that due to phenylephrine. The output of lysozyme produced by methacholine or phenylephrine was not significantly changed by PHI. 4. NPY enhanced the volume output of mucus produced by methacholine or phenylephrine; however, the rate of output of lysozyme in mucus produced by both agonists was reduced by NPY. 5. We suggest that PHI has no effect on serous cell secretion but inhibits secretion from another source, possibly mucous cells. NPY inhibits serous cell secretion but has a stronger stimulant action on secretion from another source, again possibly mucous cells. 6. PHI and NPY may be important physiological modulators of mucus volume output in the ferret trachea.

Animals↗

PubMed1989

Actions of bradykinin and related peptides on rabbit coeliac artery rings.

1. Rabbit coeliac artery rings were mounted in tissue baths containing Krebs solution at 37 degrees C in order to determine whether their response to bradykinin is initiated by B1- or B2-receptors. Tension was recorded isometrically. 2. Phenylephrine contracted the tissue. Subsequent addition of bradykinin or des Arg10-kallidin caused relaxation which was not dependent on an intact endothelium. Des Arg10-kallidin, a B1-receptor selective agonist, was more potent than bradykinin. 3. [beta-Thienyl alanyl6,9, D-Phe8]-kallidin and [Leu9]-des Arg10-kallidin antagonized bradykinin and des Arg10-kallidin. [Leu9]-des Arg10-kallidin, a B1-receptor selective antagonist, was more potent than [Thi6,9, D-Phe8]-kallidin, a less selective drug that acts on both B1- and B2-receptors. 4. Kinin-induced relaxation was reversibly antagonized by ibuprofen (a cyclo-oxygenase inhibitor) and by 5-(N,N-hexamethylene)amiloride (an inhibitor of Na+/H+ exchange). Ibuprofen caused a parallel shift to the right of a semi-logarithmic plot of the agonist concentration-effect relationship, whereas the amiloride analogue depressed the maximum response and reduced the slope. 5. We conclude that bradykinin and des Arg10-kallidin relax rabbit coeliac artery by combining with B1-receptors. The response is mediated by a cyclo-oxygenase product and may be influenced by cellular Na+/H+ exchange.

Animals↗