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At least 685 records · Page 38Linked to original sources
PubMed1987

Spectrophotometric determination of cation concentrations in olfactory mucus.

Spectrophotometric techniques were used to determine the concentrations of Na+, K+ and Ca2+ in the olfactory mucus of frogs. The mean concentrations in mEq/l were: [Na+], 52.7 +/- 4.1; [K+], 10.6 +/- 1.9 and [Ca2+], 10.7 +/- 1.7. Topical application of the odorant cineole was associated with statistically significant increases in [Na+] and [Ca2+]; the secretagogues methacholine and isoproterenol induced transient increases in [Na+]. Cineole and methacholine caused sustained increases in [Na+]/[K+] from the control value of 5:1, while isoproterenol caused a transient increase followed by a decline. The results indicate that the cation concentrations in olfactory mucus samples are more similar to those derived from secretory tissue than to those found in the extracellular fluids surrounding typical neural tissue.

Animals↗
PubMed1982

The three-ion test for the identity of the ionophores mediating the hyperpolarizing response to cholinomimetics in neurones of Helix aspersa.

1. The hyperpolarizing response investigated is mediated by Cl- ions. Additional anions NO-3 and BrO-3 were introduced into the perfusate to produce a system with 3 permeant anions. 2. Under such circumstances the reversal potential (Er) becomes a means of discriminating between the molecular mechanisms invoked by different agonists that produce an increase in anionic conductance. 3. A statistically significant difference of 0.49 mV was detected between the Er for acetylcholine and those for acetyl-beta-methyl choline and tetramethylammonium (acetylcholine more negative). 4. This difference was not significantly affected by changing to a different 3-ion solution. 5. It is argued from theoretical grounds that a change in this difference is to be expected when molecular mechanisms differ; alternative explanations for the difference are suggested.

Acetylcholine↗
PubMed1986

M1 and M2-muscarinic receptors in the epididymal half of the rat vas deferens.

The inhibitory effects of atropine and pirenzepine (nonselective and M1-selective antagonists, respectively) on the contractile responses of the epididymal half of the rat vas deferens to methacholine included a depression of the maximal response. In the presence of pirenzepine, atropine was a competitive antagonist of the responses to methacholine. However in the presence of atropine, pirenzepine remained a non-competitive inhibitor of the response. It is suggested that low concentrations of methacholine predominantly stimulate M2-receptors and that at high concentrations, methacholine also stimulates M1-receptors.

Animals↗
PubMed1987

Sr2+ may differentiate high and low affinity Ca2+ stores in guinea-pig trachealis.

1. In guinea-pig trachealis Ca2+ are mobilized from different stores to produce the contractions to various agents. 2. Sr2+ can substitute for Ca2+ and maintain responses to KC1 but not responses to A23187 or agents acting via drug-receptor interaction. 3. Resting tone and responses to KC1 are supported by low affinity Ca2+. 4. Responses to the other agents are supported by high affinity Ca2+.

Animals↗
PubMed1987

Effect of chronic administration of haloperidol on secretory response mediated by cholinergic receptors in rat submandibular glands.

Administration of haloperidol influences peripheral non-dopaminergic receptors. The sialagogue response of the submandibular glands of the rats to methacholine was enhanced by chronic administration of haloperidol. The binding of [3H]QNB to muscarinic receptors in the submandibular glands was not changed by chronic haloperidol. The supersensitivity of postsynaptic cholinergic receptors to drugs in haloperidol treated rats is not related to changes in the number or affinity of such receptors. This paper confirmed the sialagogue supersensitivity to adrenergic drugs related to an increase in alpha 1-adrenoceptors in the submandibular glands of haloperidol injected rats.

Animals↗
PubMed1988

Concentration-related differences in the effects of the Ca2+ agonist Bay K 8644 in human bronchus in vitro.

1. In human isolated bronchial muscle Bay K 8644 (1 nM-1 microM) increased the force of contraction. In concentrations greater than 1 microM (in sensitized tissues), and 10 microM (in control), Bay K 8644 relaxed tissues to below their pretreatment baseline tension. 2. In control tissues contracted with methacholine or LTD4, Bay K 8644 (10 microM) produced a further small contraction; Bay K 8644 (100 microM) relaxed the tissues below baseline. 3. In tissues contracted with histamine, Bay K 8644 (10-100 microM) produced only relaxation. 4. Bay K 8644 therefore has both Ca2+ agonist and Ca2+ antagonist properties, the calcium agonist activity is more pronounced in sensitized tissues.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

Increase of muscarinic cholinergic receptors in the rat submandibular glands after parasympathectomy and repeated administration of haloperidol.

1. The mechanisms of the supersensitivity to cholinergic drugs after chronic haloperidol was studied in normal and parasympathectomized submandibular glands of the rats. 2. Both parasympathectomy and haloperidol treatment for 7 days (2 mg/kg/day, i.p.) increased the sialogogue response of the glands to methacholine, a cholinomimetic drug. 3. Both denervation and haloperidol administration induce up-regulation of the muscarinic receptors as expressed per gram of the tissue. 4. Haloperidol causes no further increase in sensitivity than denervation alone. 5. These data demonstrate that secretory supersensitivity to cholinergic drugs in the rat submandibular glands, after chronic haloperidol and parasympathectomy is related to an increase in muscarinic cholinergic receptors.

Animals↗
PubMed1990

Effects of inhibitors of eicosanoid synthesis in the uterus of ovariectomized rats and rats in natural oestrus: relation with calcium.

1. The effects of 4 inhibitors of eicosanoid synthesis (ESIs)--mepacrine (MEP, 10(-5) - 3 x 10(-4) M), nordihydroguaiaretic acid (NDHGA, 10(-6) - 2 x 10(-5) M), indomethacin (IND, 2 x 10(-6) M and 2 x 10(-5) M) and imidazole (IMI, 10(-5) M and 10(-4) M)--on the motility induced by oxytocin (OT, 0.5 and 4 mU/ml) in uterus of rats in natural oestrus and of ovariectomized rats have been studied. 2. MEP, NDHGA and IND, but not IMI, inhibited the motility induced by both concentrations of OT in natural oestrus. Ovariectomy enhanced the effects of all ESIs, except the one of MEP. 3. MEP and NDHGA, but not IND or IMI, inhibited the contractions induced by methacholine (10(-5) M) and prostaglandin F2a (10(-6) M) and relaxed in a dose-dependent way the tonic component of the contractile response to KCl 60 mM (DI50: 6.14 +/- 0.38 and 1.38 +/- 0.29 x 10(-5) M, respectively). 4. CaCl2 (0.1-10 mM) reverted the relaxation of KCl contractions produced by MEP but not by NDHGA.

Animals↗
PubMed1991

Mechanisms involved in the effects of phenidone, diclofenac and ethacrynic acid in rat uterus in vitro.

1. The effects of phenidone (P, 10(-4)-10(-3) M), sodium diclofenac (D, 10(-5)-10(-4) M) and ethacrynic acid (E, 10(-5)-10(-4) M), proposed as inhibitors of eicosanoid synthesis, on the contractions of rat uterus induced by several agonists have been studied. 2. P, D and E inhibit the motility induced by oxytocin (4 mU/ml) (IC50: 4.62 x 10(-4), 2.55 x 10(-4) and 2.98 x 10(-5) M, respectively). 3. P (10(-3) M), D (10(-4) M) and E (10(-4) M) also inhibit the contraction induced by methacholine (10(-5) M), prostaglandin F2a (10(-6) M) and CaCl2 (6 mM), and relaxed, in a dose-dependent way, the tonic component of contraction to KCl (60 mM) (IC50: 5.81 x 10(-4), 6.67 x 10(-5) and 7.55 x 10(-5) M, respectively). 4. The CaCl2 (0.1-10 mM) reverted the relaxation of KCl contraction produced by P, but not by D or E. None of the inhibitions on CaCl2 (6 mM) are reverted by Bay K 8644. 5. D and E also relaxed the tonic contraction to vanadate (10(-4) M) in uterus incubated in calcium free solution P, enhances the vanadate-induced contractions.

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

Calcitonin gene-related peptide in rat salivary glands: neuronal localization, depletion upon nerve stimulation, and effects on salivation in relation to substance P.

Calcitonin gene-related peptide (CGRP)-immunoreactive nerve fibres occurred predominantly around blood vessels and large ducts and, to a minor extent, around acini and small ducts in the parotid, sublingual and submaxillary glands of the rat. Double immunostaining showed most of the CGRP-containing nerve fibres to contain substance P. However, the vast majority of substance P-immunoreactive periacinar nerve fibres in the parotid and submandibular glands lacked CGRP. After parasympathetic denervation of the parotid gland by section of the auriculotemporal nerve these periacinar substance P-immunoreactive nerve fibres disappeared almost completely, whereas the number of substance P/CGRP-immunoreactive nerve fibres seemed unchanged. After this operation the total amount of substance P in the parotid gland was reduced by about 90% as judged by radioimmunoassay; in denervation experiments the facial nerve was found to contribute to the residual substance P content. In contrast, the contribution of the auriculotemporal nerve to the CGRP content of the gland was small; the reduction in CGRP after section of the nerve was 20%. The facial nerve and the dorsal root nerves (C3 and C4) contributed to the CGRP content with about 50%. The source of the remaining 30% of the parotid gland CGRP is unknown. It is not the sympathetic nerve: sympathetic denervation resulted in a marked increase in CGRP, regardless of whether the auriculotemporal nerve was intact or not. Upon long-lasting electrical stimulation of the auriculotemporal nerve at a high frequency the parotid gland content of CGRP was gradually reduced, indicating depletion of this peptide in response to nerve stimulation. Intravenous injections of CGRP evoked no salivary flow; however, a release of amylase was revealed. Also, when CGRP was tested on isolated parotid gland lobules amylase was released into the medium. When, in vivo, CGRP was injected in combination with substance P, the substance P-evoked flow of parotid and submaxillary saliva was markedly enhanced. In addition, CGRP enhanced the in vivo secretory response to parasympathomimetics and to vasoactive intestinal peptide. The localization of CGRP-containing nerve fibres suggests that CGRP is involved in the regulation of secretion and blood flow of salivary glands. CGRP may interact positively with acetylcholine and certain nonclassical transmitters, and it may be involved (together with other neuropeptides) in the atropine-resistant parasympathetic secretion occurring in the glands under study.

Amylases↗
PubMed1983

Contractions in bronchial musculature of rabbit and man in response to various drugs.

1. The contractile behaviour of rabbit and man bronchial musculature has been tested in response to some commonly used substrates for cholinesterase, histamine and adrenaline by the kymograph technique. 2. The sensitivity of the smooth bronchial musculature from both rabbit and man was found to be highest for acetylcholine and acetyl-beta-methylcholine (6.3 X 10(-8) M) and lowest for butyrylcholine (6.3 X 10(-6) M). 3. The smooth bronchial musculature of man was slightly more sensitive to histamine and adrenaline than that of the rabbit. 4. The results indicate that the contractile behaviour in the smooth bronchial musculature of rabbit and man is remarkably similar.

Acetylcholine↗
PubMed1987

Cholinergic control of the mechanical properties of the catch connective tissue in the holothurian body wall.

Effects of acetylcholine (ACh), ACh-agonists and antagonists were studied on the viscosity of the dermis of the sea cucumber Holothuria leucospilota. ACh and nicotinic agonists caused an early increase in viscosity and late decrease. Muscarinic agonists produced a viscosity decrease. The viscosity increase elicited by nicotine was inhibited by tubocurarine. The viscosity decrease caused by methacholine was suppressed by atropine. The mechanical properties of this connective tissue are very likely controlled by both nicotinic and muscarinic cholinoreceptors.

Acetylcholine↗
PubMed1989

Role of phosphoinositide metabolism in functional antagonism of airway smooth muscle contraction by beta-adrenoceptor agonists.

Histamine and the muscarinic agonists, methacholine, oxotremorine, and McN-A-343, were used to contract guinea-pig tracheal smooth muscle preparations. Cumulative dose-relaxation curves with isoprenaline were performed subsequently. In addition, the concentration-dependent induction of phosphoinositide metabolism by the contractile agonists was measured in bovine tracheal smooth muscle. All agonists were found to induce a decrease of the apparent affinity of isoprenaline and a loss of relaxation, depending on the concentration and type of contractile agonist used. The differential effects of the contractile agonists, especially at higher and supramaximal concentrations, on these beta-adrenergic parameters could be explained by differences in phosphoinositide metabolism.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Agonist binding to M1 muscarinic receptors is sensitive to guanine nucleotides.

Putative M1 (high-affinity pirenzepine) muscarinic receptors in rabbit hippocampal membranes, treated with 0.1 mM N-ethylmaleimide (NEM), were selectively labeled with [3H]pirenzepine. A single class of binding sites was labeled with a Kd of 3.4 nM, consistent with the pharmacologically-defined M1 subtype of muscarinic receptors. While full muscarinic agonists bound to high- and low-affinity states of [3H]pirenzepine-labeled M1 sites with a KL/KH ratio of approximately 100, the ratio for partial muscarinic agonists was approximately 10. The high-affinity binding of all agonists tested required divalent cations, and was interconverted to low-affinity binding in the presence of the non-hydrolyzable GTP analogue, guanylyl imidodiphosphate (GppNHp). Direct labeling of the high-affinity agonist state of M1 receptors was achieved with 5 nM [3H]oxotremorine-M by selectively uncoupling the high-affinity agonist state of M2 (low-affinity pirenzepine) receptors with NEM. The rate of dissociation of [3H]Pxotremorine-M from M1 receptors was accelerated 6-fold by GppNHp. These results provide further evidence which suggests that putative M1 muscarinic receptors activate second messenger systems by coupling to NEM-insensitive guanine nucleotide-binding proteins.

Animals↗
PubMed1988

Dose-dependent inhibitory effect of inhaled beclomethasone on late asthmatic reactions and increased responsiveness to methacholine induced by toluene diisocyanate in sensitised subjects.

To determine whether inhaled beclomethasone, both at low and at high doses, inhibits late asthmatic reactions and the associated increase in airway responsiveness induced by toluene diisocyanate (TDI), we studied 9 sensitised subjects. Low dose beclomethasone (200 micrograms bid), high dose beclomethasone aerosol (1000 micrograms bid), and placebo were administered for 7 days before TDI inhalation challenge to each subject, according to a double-blind, crossover study design. The washout period between the treatments was at least 1 week. When the subjects were treated with placebo, forced expiratory volume in 1 sec (FEV1) markedly decreased after exposure to TDI. By contrast, high dose beclomethasone prevented the late asthmatic reaction and the low dose partially inhibited the reaction. With placebo the mean (+/- SE) value of FEV1 4 h after exposure to TDI was 2.6 +/- 0.17 L, which went to 3.3 +/- 0.12 after low dose beclomethasone, and to 3.5 +/- 0.15 L after high dose of beclomethasone (significant difference in the decrease of FEV1 in the 8 h after exposure to TDI, between treatments: F = 9.87, (P less than 0.001), After treatment with placebo or with low dose beclomethasone, airway responsiveness to methacholine increased 8 h after exposure to TDI. With placebo, the PD20 decreased from 0.66 mg (Geometric Standard Error of the Mean [GSEM], 1.38) to 0.18 mg (GSEM, 1.46); with low dose inhaled beclomethasone, the PD20 decreased from 0.93 mg (GSEM, 1.42) to 0.36 mg (GSEM, 1.63).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗