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At least 343 records · Page 19Linked to original sources
PubMed1986

Beta-2-agonists of third generation.

Beta-adrenergic agents have been used for a long time in the treatment of asthma. For the purpose of bronchodilation the better results would be attained with the increase in Beta-2-selectivity. From the newer Beta-agonists the mot currently used are TERBUTALINE, FENOTEROL, SALBUTAMOL, CLEMBUTEROL, TOLBUTEROL, CARBUTEROL, PROCATEROL, RIMITEROL and REPROTEROL, this last combining in its molecule the structure of a beta-agonist with a Xanthine group. These agents could be used in different ways, by mouth, injection and inhalation (with a exception of Clembuterol which is effective only by oral route). The authors have, some years ago, comparatively studied the bronchodilating effect of Salbutamol and Fenoterol including 18 patients. The main increase of PFR was slightly higher after FENOTEROL but this difference was not significant. The authors have studied REPROTEROL by inhalation and oral routes in 11 asthmatic patients. After inhalation of 400 mcg of REPROTEROL the bronchodilator effect was comparable to others inhaled bronchodilators. However they could not confirm that REPROTEROL acts also as a Xanthine and only traces of Theophylline have been detected in blood of subjects taking it. These data seem to indicate that REPROTEROL do not release Theophylline in the body or only release a Xanthine like compound not detected by "EMIT" of high pressure liquid chromatography.

Adrenergic beta-Agonists↗
PubMed1983

The human heart beta-adrenergic receptors. I. Heterogeneity of the binding sites: presence of 50% beta 1- and 50% beta 2-adrenergic receptors.

Beta-adrenergic receptors were characterized in a particulate fraction of human auricles obtained from patients operated upon for coronary insufficiency or valvular disease. [125I] Hydroxybenzylpindolol binding was evaluated in terms of kinetics; KD and Bmax values; and inhibition of binding in the presence of 10 microM GTP and of increasing concentrations of four nonselective agonists giving a Hill coefficient of 1 (isoproterenol, salbutamol, fenoterol, and epinephrine), of two nonselective antagonists giving a Hill coefficient of 1 (pindolol and propranolol), and of a series of selective drugs giving a Hill coefficient of 0.60-0.72 that included three beta 1-selective antagonists (practolol, metoprolol, and atenolol) and two beta 2- selective agonists (procaterol and zinterol). KD values for all drugs were compatible with the coexistence in membranes from human auricles of beta 1- and beta 2-adrenergic receptors, the relative proportions of receptors of each subclass being approximately the same.

Adrenergic beta-Agonists↗
PubMed1983

The human heart beta-adrenergic receptors. II. Coupling of beta 2-adrenergic receptors with the adenylate cyclase system.

The beta-adrenergic stimulation of adenylate cyclase in membranes from human auricles, ventricles, and fetal heart was compared with the binding properties of beta-adrenergic receptors in human auricles. In terms of adenylate cyclase activation, three full agonists (isoproterenol, epinephrine, and norepinephrine), four partial agonists (procaterol, salbutamol, fenoterol, and zinterol), and four antagonists (propranolol, metoprolol, atenolol, and practolol) were tested. The beta-adrenergic activation of adenylate cyclase in membranes from rat heart (with a majority of beta 1-adrenergic receptors), rat erythrocytes, and rat reticulocytes (with a homogeneous population of beta 2-adrenergic receptors) served as reference. The reactivity of human heart adenylate cyclase, estimated by the Kact or Ki values of 11 beta-adrenergic agents, indicated that the activation of this enzyme occurred through receptors of the beta 2-subtype only. Receptors of the beta 1-subtype (50% of the total population) were not coupled to the enzyme.

Adenylyl Cyclases↗
PubMed1984

Pharmacological studies of mabuterol, a new selective beta 2-stimulant. I: Bronchodilating effect.

The bronchodilating effect and other related pharmacological properties of dl-1-(4-amino-3-chloro-5-trifluoromethyl-phenyl)-2-tert.-butylamino-etha nol hydrochloride (mabuterol) were studied in comparison with those of isoprenaline (isoproterenol), salbutamol and procaterol. In relaxing the isolated normal tracheal muscle in guinea pigs, mabuterol was more potent than isoprenaline and salbutamol, and the effect seemed to be due to the activation of beta-adrenoceptors because it was inhibited by propranolol. In anesthetized guinea pigs, mabuterol given i.v. was less potent but showed a longer duration of action than isoprenaline and salbutamol in inhibiting an increase in the bronchial resistance induced by acetylcholine, histamine and serotonin. When given intraduodenally, it was 1.9-7.8 times more potent than isoprenaline and salbutamol. In conscious guinea pigs, mabuterol given subcutaneously was less potent than isoprenaline and salbutamol in experimental asthma induced by acetylcholine, histamine and antigen, but 26-102 times more potent than the reference bronchodilators when given orally. Chronic oral treatment of mabuterol showed no significant change in the inhibitory effect on the experimental asthma and no development of tolerance was observed. In the maximum increase in the heart rate in conscious guinea pigs, mabuterol given orally was less potent than isoprenaline and salbutamol. Calculation of the selectivity ratio of the drugs for the bronchial muscle vs. cardiac muscle indicated that mabuterol was about 7.4 times more selective for the bronchial muscle than salbutamol.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Reduction of the severity of bronchial hyperresponsiveness by the novel leukotriene antagonist 4-oxo-8-[4-(4-phenyl-butoxy)benzoylamino]-2- (tetrazol-5-yl)-4H-1-benzopyran hemihydrate.

There is much evidence that the cysteinyl-leukotrienes (C-LTs) are important in the pathogenesis of asthma. The clinical effect of a new leukotriene antagonist, ONO 1078 (4-oxo-8-[4-phenylbutoxy)benzoylamino]-2-(tetrazol-5-yl)-4H- 1-benzopyran hemihydrate, CAS 103177-37-3) on symptoms, pulmonary lung function and bronchial hyperresponsiveness was evaluated in patients with bronchial asthma. Eleven patients were treated for 24 weeks with 450 mg of ONO 1078 twice daily. The score of asthma symptom severity and the number of inhaled procaterol were significantly reduced after 2 weeks of ONO 1078 treatment and remained decreased for another 22 weeks. Their FEV1 and PC20 to histamine significantly improved 12 and 24 weeks after ONO 1078 treatment. The effectiveness of ONO 1078 suggests that the C-LTs play an important role in the pathogenesis of asthma. ONO 1078 might help to favorably modify the pathophysiologic condition in patients with bronchial asthma.

Adult↗
PubMed1994

[A case of bronchial asthma associated with reflux esophagitis, whose peak expiratory flow rate improved with omeprazole and cisapride].

A 60-year-old male had visited our hospital periodically, because of perennial moderate atopic asthma, since 53 years of age. His symptoms had stabilized following treatment with oral theophylline 400 mg, tranilast 300 mg and inhalation of beclomethasone dipropionate 400 micrograms and procaterol hydrochloride. His peak expiratory flow rate early in the morning was 465 L/min, %VC was 115% and FEV1.0% was 62.4% in May of 1993. On May 24, 1993, though he had no gastrointestinal symptoms, gastrointestinal fiberscopy revealed a hiatal hernia, reflux esophagitis and active gastroduodenal ulcer. The upper gastrointestinal x-ray films showed gastroesophageal reflux. Therefore, we diagnosed bronchial asthma associated with reflux esophagitis and gastroduodenal ulcer. He was started on omeprazole, as a proton pump inhibitor (PPI), and cisapride. After the treatment with PPI and cisapride, his peak expiratory flow rate early in the morning and in the evening, %VC and FEV1.0 increased. Three months later gastrointestinal fiberscopy revealed improvement in the reflux esophagitis and the gastroduodenal ulcer. We speculate that the improvement in the peak expiratory flow rate is related to that of the gastroesophageal reflux.

Asthma↗
PubMed1993

[A case of allergic bronchopulmonary candidiasis improved with steroid inhalation].

A 49-year-old woman was admitted to hospital because of productive cough and dyspnea. She had been well two months before admission, when she developed an attack of asthma. Chest roentgenogram taken on admission revealed numerous shadows of inhomogeneous density in both lungs. Laboratory findings showed leukocytosis with eosinophilia (25%), high IgE level in serum and positive RAST score to Candida albicans. A diagnosis of allergic bronchopulmonary candidiasis was made by these laboratory data and clinical course. The patient was treated successfully by oral administration of methylprednisolone and inhalation of amphotericin B, but she had a relapse of the disease on cessation of steroid medication. Inhalation of beclomethasone dipropionate and procaterol hydrochloride was commenced. Thereafter, pulmonary infiltration and clinical symptoms improved after three weeks.

Administration, Inhalation↗
PubMed1997

[Cough-variant asthma successfully treated with a peptide leukotriene receptor antagonist].

A 47-year-old woman complained of coughing for over 5 weeks. The coughing was not relieved by bronchodilators (theophylline, beta 2-adrenoceptor agonist; procaterol), anti-allergic agents (azelastine, ozagrel), an inhaled corticosteroid (beclomethasone dipropionate), a macrolide antibiotic (clarithromycin), or codeine phosphate. A peptide leukoriene receptor antagonist (pranlukast) completely abolished the coughing and increased the cough threshold to capsaicin. The patient was given a diagnosis of cough-variant asthma because her sputum contained many eosinophils and her airway responsiveness to methacholine was slightly higher than normal. Peptide leukotriene may have contributed to the coughing. The fact that coughing associated with cough-variant asthma was abolished by a peptide leukotriene receptor antagonist is clinically important.

Anti-Asthmatic Agents↗
PubMed1998

[Bronchodilator aerosol propellant interferes with an photoacoustic spectrophotometer respiratory gas analyzer].

A patient with bronchial asthma was scheduled for an operation under nitrous oxide-isoflurane anesthesia. We monitored isoflurane concentrations continuously using an anesthetic gas analyzer (BK 1304). Upon puffing procaterol hydrochloride aerosol for 4 times, the analyzer showed a rapid increase in end-tidal isoflurane concentration. The BK 1304 uses infrared photoacoustic spectrophotometry and it is susceptible to interferences caused by Freon propellants in bronchodilator aerosols. We should take care in monitoring inhalational anesthetics when using aerosols containing Freon propellants.

Aerosols↗
PubMed1990

Selective binding of ligands to beta 1, beta 2 or chimeric beta 1/beta 2-adrenergic receptors involves multiple subsites.

The molecular basis of ligand binding selectivity to beta-adrenergic receptor subtypes was investigated by designing chimeric beta 1/beta 2-adrenergic receptors. These molecules consisted of a set of reciprocal constructions, obtained by the exchange between the wild-type receptor genes of one to three unmodified transmembrane regions, together with their extracellular flanking regions. Eight different chimeras were expressed in Escherichia coli and studied with selective beta-adrenergic ligands. The evaluation of the relative effect of each chimeric exchange on ligand binding affinity was based on the analysis of delta G values, calculated from the equilibrium binding constants, as a function of the number of substituted beta 2-adrenergic receptor transmembrane domains. The data showed that the contribution of each exchanged region to subtype selectivity varies with each ligand; moreover, while several regions are critical for the pharmacological selectivity of all ligands, others are involved in the selectivity of only some compounds. The selectivity displayed by beta-adrenergic compounds towards beta 1 or beta 2 receptor subtypes thus results from a particular combination of interactions between each ligand and each of the subsites, variably distributed over the seven transmembrane regions of the receptor; these subsites are presumably defined by the individual structural properties of the ligands.

Adrenergic beta-Agonists↗
PubMed1985

Computer-assisted analysis of complex concentration-response data.

The analysis of concentration-response data generally relies on graphic techniques to gain estimates of the EC50, maximum response, and Hill coefficient. This type of analysis may be adequate if the drug-mediated response follows the simple mass action law; however, if the drug produces a complex concentration-response relationship through multiple receptor activation this type of analysis can give misleading information regarding the potency and actions of the particular agonist being tested. In addition, graphic analytical techniques can mask potentially useful information. There are, however, many computer programs currently available that can adequately analyze complex concentration-response data by use of weighted nonlinear curve-fitting techniques. The present paper reports on the use of some of these programs (e.g., FUNFIT and LIGAND) and how they might be used to analyze results obtained from experiments where multiple receptor activation occurs. The use of these programs gives more accurate estimates of the required constants and, in addition, can provide useful information regarding the process that produces the complex data.

Animals↗
PubMed1995

Desensitization of beta-adrenergic responses in adipocytes involves receptor subtypes and cAMP phosphodiesterase.

Acute exposure of isolated adipocytes to isoproterenol induces the desensitization of lipolytic responses to norepinephrine and selective beta 1-, beta 2- and beta 3-adrenoceptor agonists, as well as the adrenocorticotropic hormone 1-24 fragment (ACTH). Forskolin and 8-bromo-cAMP responses are also desensitized. When lipolysis was measured in the presence of OPC 3911 [N-cyclohexyl-N-2-hydroxyethyl-4(6-(1,2-dihydro-2- oxoquinolyloxy))butyramide], a specific inhibitor of the cAMP phosphodiesterase of adipocytes, the desensitization of all lipolytic agents--except the beta 2-adrenoceptor agonist--was abolished. Isoproterenol induced a similar loss (35%) of both membrane beta 1- and beta 2-adrenoceptors and an uncoupling of beta 1-adrenoceptors, but did not modify the weak coupling of control beta 2-adrenoceptors. These data suggest that isoproterenol induced (i) an activation of the cAMP phosphodiesterase, which is solely responsible for the desensitization of norepinephrine response as well as beta 1- and beta 3-adrenoceptor mediated responses and (ii) an additional desensitization of the sole beta 2-adrenergic signaling system which suggests a subtype-selective pattern of regulating processes.

Adipocytes↗
PubMed2004

3,3',4,4',5-Pentachlorobiphenyl (PCB 126) impacts hepatic lipid peroxidation, membrane fluidity and beta-adrenoceptor kinetics in chick embryos.

Polychlorinated biphenyls (PCB) and other aryl hydrocarbon receptor (AHR) agonists induce oxidative stress and alter membrane lipid peroxidation and fluidity. This study tested the hypothesis that PCB-induced changes in membrane properties impact membrane beta-adrenoceptor (beta-AR) affinity and capacity in chick embryo hepatocytes. Embryos were injected into the air cell with 1.6 microg 3,3',4,4',5-pentachlorobiphenyl (PCB 126)/kg egg at day 0, and incubated to day 19 when livers were removed. This dose resulted in hepatic PCB 126 levels of 0.67 ng/g liver or 10.2 ng/g liver lipid; levels in untreated embryos were non-detectable. Hepatic microsomal EROD activity was elevated by approximately 12-fold and embryo mortality was significantly increased compared with the untreated group. Hepatic lipid peroxidation increased and membrane order (steady-state fluorescence anisotropy values) decreased with in ovo PCB 126 exposure. Consistent with changes in membrane structure, hepatic beta-AR affinity for CGP 12177 significantly decreased (Kd increased) without changes in receptor numbers. This study demonstrates that in ovo exposure to PCB 126 in chick eggs significantly impacted embryo survival, and this was correlated with altered hepatic membrane structure and ultimately membrane function.

Adrenergic beta-Agonists↗
PubMed2006

Cathine, an amphetamine-related compound, acts on mammalian spermatozoa via beta1- and alpha2A-adrenergic receptors in a capacitation state-dependent manner.

BACKGROUND: Mammalian spermatozoa have been shown to have beta(1,2,3)- and alpha(2A)-adrenergic receptors, the former functioning only in uncapacitated spermatozoa and the latter only in capacitated cells. Cathine, an amphetamine-related metabolite of a compound found in Catha edulis leaves, accelerates capacitation and inhibits spontaneous acrosome loss by regulating cAMP production. This study tested the hypothesis that adrenergic receptors are involved in these responses. METHODS: Uncapacitated and capacitated mouse sperm suspensions were incubated with cathine +/- specific antagonists for alpha(2)- and beta-adrenergic receptors for 35 min, then assessed using chlortetracycline fluorescence. Reversibility of receptor accessibility was assessed by depleting suspensions of endogenous decapacitation factor (DF) and then adding crude DF with/without cathine and antagonists. Effects on tyrosine phosphorylation and calcium requirements for both ligand binding and biological responses were also evaluated. RESULTS: Cathine's acceleration of capacitation was blocked by a beta(1)-antagonist, whereas an alpha(2)-antagonist blocked inhibition of acrosome reactions. Cathine accelerated capacitation in decapacitated cells, a response inhibited by a beta(1)-antagonist; cathine also stimulated tyrosine phosphorylation. Although calcium was not required for binding, it was needed for responses. CONCLUSIONS: Cathine acts at beta(1)-adrenergic receptors in uncapacitated spermatozoa and at alpha(2A)-receptors in capacitated cells; biological activity requires calcium but binding does not. Adrenergic receptor-binding sites can be made reversibly accessible/inaccessible by changing the capacitation state of spermatozoa. These results suggest that amphetamine-related compounds might enhance chances of fertilization in vivo.

Adrenergic beta-1 Receptor Agonists↗
PubMed1989

Function, characterization and autoradiographic localization and quantitation of beta-adrenoceptors in cardiac tissues.

1. This paper demonstrates the use of organ bath, radioligand binding and autoradiography to detect beta 1- and beta 2-adrenoceptors in human and guinea-pig cardiac tissues. 2. In organ bath experiments, non-selective and beta 1- and beta 2-adrenoceptor selective agonists produced concentration-dependent inotropic responses in human right atrial appendage. Both subtypes mediate inotropic responses. In guinea-pig right atria chronotropic responses were mediated predominantly through beta 1-adrenoceptors. 3. Receptor binding studies using (-)[125I]-cyanopindolol (CYP) and beta 1- and beta 2-adrenoceptor selective antagonists showed that beta 2-adrenoceptors comprised 25% of the total population of beta-adrenoceptors in guinea-pig right atria. In human right atria the proportion is higher (40%). 4. Quantitative autoradiography was used to determine the location and densities of beta 1- and beta 2-adrenoceptors in guinea-pig heart. Both beta 1- and beta 2-adrenoceptors were distributed on myocardium. The atrioventricular conducting system had a higher density of beta 2-adrenoceptors compared with myocardium.

Adrenergic beta-Agonists↗
PubMed1997

Leukotriene antagonist prevents exacerbation of asthma during reduction of high-dose inhaled corticosteroid. The Tokyo Joshi-Idai Asthma Research Group.

To test whether the leukotriene antagonist ONO-1078 (pranlukast) prevents asthma exacerbations during reduction of high-dose inhaled corticosteroid, we conducted a randomized, double-blind, placebo-controlled study in 79 asthma patients requiring high doses (1,500 microg/d or more) of inhaled beclomethasone dipropionate (BDI) for clinical control (duration of asthma, 11.0 +/- 3.1 yr; duration of BDI treatment, 0.5 +/- 0.3 yr; FEV1 percentage of predicted, 80.7 +/- 2.0%). After a 2-wk run-in period, the doses of BDI were halved, while the patients were assigned to receive orally ONO-1078, 450 mg twice daily, or placebo. In the placebo group FEV1 decreased by 0.33 +/- 0.20 L after 6 wk (p < 0.001). Likewise, morning and evening PEF decreased by 46 +/- 7 L/min and 18 +/- 6 L/min, respectively. By contrast these variables were sustained above baseline in the ONO-1078 group. The number of daytime and nighttime asthma symptoms and the use of beta2-agonist increased in the placebo group, whereas they remained unchanged in the ONO-1078 group. In the placebo group concentrations of serum eosinophil cationic protein and exhaled nitric oxide increased (p = 0.007 and p = 0.025, respectively), compared with no change in the ONO-1078 group. Therefore, the leukotriene antagonist ONO-1078 prevents the asthma deterioration provoked by a 6-wk reduction of the dose of inhaled BDI into half.

Administration, Inhalation↗