PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Methacholine Compounds”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1983

Intraspecies variation in methacholine-stimulated esterase release from mouse submandibular gland.

Esterase release was investigated in male and female submandibular glands of 5 strains of mice (ICR/BR, ND/4BR, SW/BR, DDS/Cox and C57BL/6BR) using dispersed cells prepared by treatment with collagenase and hyaluronidase. The muscarinic-cholinergic agonist methacholine stimulated esterase release in C57BL/6BR, DDS/Cox and SW/BR females and DDS/Cox males in a dose-dependent manner, but did not stimulate esterase release in ICR/BR and ND/4BR strains of both sexes. The percentage release of esterase over control in response to methacholine in females was of the descending order: C57BL/6BR, DDS/Cox, SW/BR, ND/4BR, ICR/BR. There was a close relationship between the percentage release of esterase by methacholine and the esterase activity in homogenate of submandibular gland. The lower the esterase content in the homogenate of mouse submandibular gland, the higher the percentage release of esterase by methacholine stimulation in the dispersed cells.

Animals↗
PubMed1984

Methacholine-stimulated release of benzoyl-arginine-ethylester esterase from mouse submandibular gland cells.

The possible existence of cholinoceptor for inducing benzoyl-arginine-ethylester (BAEe) esterase release in the mouse submandibular gland was investigated using dispersed-cell preparations from normal male and female, castrated male and testosterone-treated female mice. Methacholine (a cholinoceptive agonist) induced esterase release only in normal female and castrated male mice, both of which had low esterase activity in the submandibular glands, whereas norepinephrine (an alpha-adrenoceptor agonist) induced esterase release in all of the mice. Methacholine-induced esterase release was completely inhibited by atropine, a cholinoceptive antagonist, but not by phenoxybenzamine, an alpha-adrenoceptor antagonist. The effects of metacholine and norepinephrine on esterase release were additive. The results suggest the coexistence of cholinoceptor and alpha-adrenoceptors for esterase release in the mouse submandibular gland. Calcium was essential for esterase release induced by either methacholine or norepinephrine.

Animals↗
PubMed1985

Amylase in parotid saliva of rats after sympathetic nervous decentralization.

The marked increase in the amylase secretion that occurs in parasympathetic saliva some days after sympathetic ganglionectomy occurred after decentralization also; hence, it results from lack of impulses from the central nervous system. It occurred whether salivation was evoked by activating muscarinic receptors with methacholine, peptidergic receptors with substance P or physalaemin, or alpha-adrenoceptors with phenylephrine. Unilateral operation affected to some degree the contralateral gland also.

Amylases↗
PubMed1989

Effects of cadmium on the function and structure of the rat salivary glands.

The effects of sub-chronic cadmium (Cd) administration on the structure and subsequent secretory responses of the submaxillary and parotid glands to sialagogues were investigated. Female Wistar rats were injected subcutaneously with cadmium chloride (3.0 mg/kg body weight), 4 times a week for 2, 3 or 4 weeks. Functional and histopathological studies were done 3 days after the last injection. Dose-response curves for norepinephrine and methacholine were obtained. After 2 weeks of Cd administration significant changes in the secretory response to these sialogogues were observed. The dose-response curves after pretreatment with Cd for 3 weeks were also shifted to the right, but the response showed recovery when compared with that of 2-week treated animals. Parotid amylase concentration was also diminished by Cd. Treated rats had reduced acinar diameters, and an increase in acinar cell nuclei per field in both the submaxillary and parotid glands. Thus sub-chronic administration of ionized Cd produces morphological and functional changes in rat salivary glands. Moreover, the extent of tubular and acinar damage matches the degree of gland dysfunction as judged by the diminution of secretory responses to sialagogues.

Amylases↗
PubMed1989

Secretion of amylase from the rat parotid salivary gland after degeneration of the auriculotemporal nerve.

The output of amylase into saliva secreted after injection of methacholine or substance P was increased after parasympathetic denervation, but the salivary concentration of amylase was unchanged. The increased output corresponded to the increased flow. Isoprenaline injected during the methacholine-induced secretion raised the output, more being secreted from the denervated than from the contralateral gland. Vasoactive intestinal peptide, given while substance P caused salivation, also increased the amylase output, but equally from the two glands.

Amylases↗
PubMed1975

Myocardial guanylate cyclase: properties of the enzyme and effects of cholinergic agonists in vitro.

The characteristics of myocardial guanylate cyclase (GTP pyrophosphatelyase, EC 4.6.1.2) were studied. Specific activity of the myocardial enzyme in five vertebrate species was guinea pig greater than man greater than cat greater than dog greater than rat. In the guinea pig, guanylate cyclase activity was uniformly distributed throughout the anatomical regions of the heart. The major portion of the enzyme activity was retrieved in the supernatant fraction after centrifugation at 12 000 times g. The Km for GTP was similar in supernatant (0.12 mM) and particulate (0.21 mM) preparations, although the Ka for Mn2+ in particulate preparations (0.3-0.6 mM) was less than that observed for guanylate cyclase in the supernatant fraction (0.8-2.0 mM). ATP competitively inhibited supernatant and particulate activity. Addition of 0.005-10.0 mM Ca2+ to assay incubations did not enhance guanylate cyclase activity. Suspension of 105 000 times g supernatant guanylate cyclase preparations with membrane lipids or phosphatidylserine stimulated activity 1.4-4.3 fold, whereas similar treatment of particulate preparations caused little alteration of enzyme activity. Addition of the cholinergic agonists acetylcholine, carbachol or methacholine (10-4-10-8 M) to homogenate, supernatant, particulate and disrupted tissue slice preparations in the presence of 0.0012-1.2 mM GTP, 0.3-10.0 mM Mn2+ and 0.005-10.0 mM Ca2+ or 0.0012-1.2 mM ATP did not stimulate guanylate cyclase activity. Similarly, further stimulation of guanylate cyclase activity was not elicited when enzyme-lipid suspensions were assayed in the presence of cholinergic agents.

Acetylcholine↗
PubMed1987

Effect of platelet-activating factor on beta-adrenoceptors in human lung.

We examined the effect of platelet-activating factor (PAF) on beta-adrenoceptors in the membranes of human lung and the functional responses to methacholine, histamine and isoproterenol in human lung parenchyma and tracheal strips. Preincubation of the human lung slices with 0.1 microM PAF decreased the density of beta-adrenoceptors without a change in the affinity. In the functional studies, a subthreshold dose of PAF (0.1 microM) significantly reduced the potency of isoproterenol to reverse methacholine or histamine-induced contraction. BN 52021, a PAF antagonist, protected against these PAF-induced changes. These findings suggest that PAF-induced down-regulation of beta-adrenoceptors could be a mechanism of the non-specific airway hyperreactivity in asthma.

Cell Membrane↗
PubMed1987

A disbalance between beta-adrenergic and muscarinic responses caused by hydrogen peroxide in rat airways in vitro.

The effect of hydrogen peroxide on adrenergic and muscarinic responses of rat airway smooth muscle was studied. The trachea muscle and the lung parenchymal strip were contracted with methacholine and relaxed with (-)-isoprenaline. Recording of three (-)-isoprenaline curves on the trachea muscle and the lung parenchymal strip was followed by treatment for 30 min with hydrogen peroxide (H2O2) (1mM) after which a new dose response curve for (-)-isoprenaline was constructed. Using the trachea muscle this treatment with H2O2 resulted in a decrease of 61% of the maximum contraction by methacholine compared with the control and a complete inhibition of the relaxation by (-)-isoprenaline. In the lung parenchymal strip preparation we found, after the same treatment no reduction of the contraction by methacholine and 61% reduction of the relaxation by (-)-isoprenaline, compared with the control. The results demonstrate that the adrenergic response in rat airways is more susceptible to hydrogen peroxide than the muscarinic response.

Animals↗
PubMed1989

Formation of chloramine derivatives of histamine: role of histamine chloramines in bronchoconstriction.

Hypochlorous acid generated by myeloperoxidase reacts with histamine to produce chloramines. At pH 7, one mole of histamine monochloramine (HisCl) was generated per mole of H2O2 provided as substrate for myeloperoxidase. At pH 5, one mole of histamine dichloramine (HisCl2) was generated per two moles of H2O2. HisCl and HisCl2 had two and four oxidizing equivalents per molecule, respectively. In vitro, 30 microM HisCl and HisCl2 induced mepyramine-sensitive guinea pig lung parenchyma contraction with 89 and 56 percent of the response of an equivalent concentration of histamine. Pretreatment of lung strips with chloramines reduced the subsequent contractile response of the tissues to methacholine. These results suggest that H-1 histamine receptors provide for targeting of histamine chloramines to pulmonary tissue which may facilitate modification of tissue responses.

Animals↗