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PubMed1983

Coexistence of beta 1- and beta 2-adrenoceptors in human right atrium. Direct identification by (+/-)-[125I]iodocyanopindolol binding.

The highly specific beta-adrenoceptor radioligand, (+/-)-[125I]iodocyanopindolol, has been used to subclassify beta-adrenoceptors in membranes from human right atrial appendage obtained during open heart surgery. Binding of (+/-)-[125I]iodocyanopindolol was saturable (Bmax = 86.4 +/- 7.4 fmol (+/-)-[125I]iodocyanopindolol bound/mg protein, n = 4), of high affinity (KD = 53 +/- 6 pM, n = 4), rapid, reversible, and stereospecific. The relative potencies of isoprenaline, adrenaline, and noradrenaline for inhibition of (+/-)-[125I]iodocyanopindolol binding and activation of adenylate cyclase were 1:10:10, indicating a population composed mainly of beta 1-adrenoceptors. Inhibition of (+/-)-[125I]iodocyanopindolol binding by beta 1- (practolol, metoprolol, betaxolol) and beta 2- (IPS 339, ICI 118,551, zinterol, procaterol) selective drugs, however, resulted in biphasic displacement curves with slope factors (nH, pseudo Hill coefficients) significantly less than 1.0. Nonlinear regression analysis of these curves revealed a beta 1: beta 2 ratio of 80:20 in human right atrial appendage. Nonselective beta-adrenergic drugs (propranolol, isoprenaline, and adrenaline), on the contrary, inhibited binding with monophasic displacement curves and nH = 1.0. Binding of agonists to the beta-adrenoceptors in human right atrial appendage seems to be regulated by guanyl nucleotides. In the absence of GTP, isoprenaline binds to high and low affinity state of the beta-adrenoceptors. GTP (10(-4) M) converts this heterogeneous binding into a homogeneous one of low affinity. It is concluded that, in human right atria, beta 1- and beta 2-adrenoceptors coexist; however, beta 1-adrenoceptors predominate. The physiological function of beta 2-adrenoceptors in human right atrium remains to be elucidated.

Adenylyl Cyclases↗
PubMed1994

Binding of a catechol derivative of denopamine (T-0509) and N-tert-butylnoradrenaline (Colterol) to beta 1- and beta 2-adrenoceptors.

The affinities for beta-adrenoceptors, the subtype-selectivity and the agonistic effectiveness of T-0509 (a catechol derivative of denopamine) and colterol (N-tert-butylnoradrenaline; Col) were compared with those of other beta-agonists using a binding assay method. Specific binding of [3H]dihydroalprenolol (3H-DHA) to guinea pig left ventricular and lung membranes was saturable, and Scatchard and Hill analyses suggested that 3H-DHA bound to both membranes with a single population of binding sites with no binding site cooperativity. Addition of 5'-guanylylimidodiphosphate (GppNHp, 30 microM) led to a rightward shift of the 3H-DHA binding displacement curves of T-0509 and Col in both membranes, and the degree of shift was similar to that of full agonists such as isoproterenol (Iso), adrenaline (Adr) and noradrenaline (NA). Both T-0509 and Col were thus considered to be full agonists at both beta 1- and beta 2-adrenoceptors, respectively, unlike denopamine and procaterol. T-0509 and Col showed considerably high affinity for both beta 1- and beta 2-adrenoceptors, and T-0509, like denopamine, was as selective for the beta 1-subtype as NA (4.5-fold compared with Iso as a non-selective agonist), whereas Col was more selective for the beta 2-subtype than Adr (4.5-fold compared with Iso).

Adrenergic beta-Agonists↗
PubMed1991

Effects of beta-adrenergic agonists on metabolic activations of human neutrophils.

Although effects of adrenergic agonists on metabolic activation of neutrophils have been studied for over a decade, amounts of released arachidonic acid and its metabolites from the cells activated by chemotactic peptide (FMLP) are so small that the results have been in conflict. In this study, we developed a method to obtain enough amount of arachidonic acid released to examine the action sites of adrenergic agonists with respects to the metabolic bursts of human neutrophils. First, superoxide generation from the cells was estimated and the results indicated that the adrenergic agonists, such as isoproterenol, salbutamol, procaterol and epinephrine, inhibited over 70% and 40% of the superoxide generation stimulated by FMLP and serum treated zymosan (STZ), respectively. Another metabolic activation, the release of arachidonic acid, was achieved by FMLP if the cells were incubated with merthiolate (20-80 microM), but the merthiolate-treatment was ineffective on the cells activated by calcium ionophore (A23187). Isoproterenol and epinephrine decreased the arachidonic acid release only when the cells were activated by FMLP in the presence of merthiolate. In spite of the fact that isoproterenol (1 and 10 microM) hardly inhibited the arachidonic acid release activated by A23187, formations of leukotrienes were decreased up to approximately 70% of control level. Intracellular calcium concentration elevated by FMLP was hardly diminished by isoproterenol and salbutamol. From these observations, it appears likely that adrenergic agonists attenuate the signal transmission process of FMLP at a post-receptor site of action at a step before the activation of protein kinase C or phospholipase A2.

Adrenergic beta-Agonists↗
PubMed1980

The tissue content of cyclic AMP in rats after microwave irradiation in vivo.

When anesthetized rats were exposed to microwave (power output 1.3 kw, frequency 2,450 MHz), the cyclic AMP phosphodiesterase activity showed a rapid decline in the skeletal muscle, heart, trachea and lung; no activity essentially could be detected after a 30 sec irradiation. Cyclic AMP levels in these tissues also decreased rapidly to constant values within 30 sec. Concentrations of cyclic AMP in the heart, skeletal muscle, trachea and lung measured by the tissue fixation with liquid nitrogen were approximately 3, 3, 4 and 4 times higher than those after microwave irradiation, respectively. The intravenous injection of procaterol (1 mu mol/kg), a beta 2-adrenoceptor agonist, caused a 6-fold increase in the trachea cyclic AMP level when measured after microwave fixation but only a 2-fold increase when measured after liquid nitrogen fixation. It is concluded that rapid tissue fixation by microwave irradiation may provide a useful means for obtaining reliable values of the tissue cyclic AMP content.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Beta 1-adrenoceptor-mediated amylase release and cyclic AMP accumulation in rat parotid gland tissue.

The present study was carried out to determine the relationship of beta 1- and Beta 2-subtype to amylase release and cyclic AMP (cAMP) accumulation in rat parotid tissue. In in vitro experiments, beta-adrenergic agents (isoproterenol and dobutamine)-induced amylase release and cAMP accumulation were all completely inhibited by the beta 1-antagonist metoprolol, but incompletely inhibited by the beta 2-antagonist butoxamine. The beta 2-agonist procaterol caused little or no amylase release or cAMP accumulation. Our results suggest that both amylase release and cAMP accumulation in rat parotid tissue may be selectively induced by beta 1-adrenergic stimulation.

Adrenergic beta-Agonists↗
PubMed1985

Hypertrophy and dysfunction of parotid gland induced by chronic stimulation of beta 1-adrenergic receptors.

The present study was carried out to determine the beta-receptor subtype responsible for the hypertrophy and dysfunction of parotid glands in rats chronically treated with isoproterenol (ISP). Treatment with dobutamine (DBT), a beta 1-agonist, (30 mg/kg twice a day for 4 days) produced a significant enlargement of the parotid gland just as in the ISP-treated rats. The effects of secretagogues on amylase release and ISP-induced cyclic AMP accumulation were markedly decreased in the parotid tissue of the treated rats. Co-administration of the beta 1-antagonists metoprolol and acebutolol clearly inhibited the development of parotid enlargement and its secretory dysfunction induced by ISP or DBT. Procaterol treatment (30 mg/kg, twice a day for 4 days) did not cause any dysfunction or any increase in the gland weights. These results indicate that both hypertrophy and dysfunction of the rat parotid gland, which were observed in chronic treatment with ISP, may result from chronic stimulation of beta 1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed2002

Characterization of beta-adrenoceptor subtype in bladder smooth muscle in cynomolgus monkey.

We first investigated the relaxations of the urinary bladder induced by beta-adrenoceptor agonists in anesthetized cynomolgus monkeys and then employed a variety of beta-adrenoceptor agonists and antagonists in vitro to identify the beta-adrenoceptor subtype responsible for the relaxation (using isolated monkey detrusors). Isoprenaline reduced bladder pressure in a dose-dependent manner. Isoprenaline, noradrenaline and adrenaline each produced a concentration-dependent relaxation of isolated detrusor strips, the rank order of relaxing potencies being isoprenaline > noradrenaline > adrenaline. Subtype-selective beta-adrenoceptor agonists also relaxed isolated detrusor strips, the rank order of potencies being CGP-12177 > BRL 37344 > dobutamine, salbutamol, procaterol > xamoterol. In the antagonist experiment, bupranolol (beta-antagonist, 10(-6) to 10(-5) M) and SR 58894A (beta3-antagonist, 10(-7) to 10(-5) M) caused a rightward shift of the concentration-relaxation curve for isoprenaline, but CGP-20712A (beta1-antagonist, 10(-9) to 10(-7) M) and ICI-118551 (beta2-antagonist, 10(-9) to 10(-7) M) did not. The present functional study provides the first evidence that relaxation of the monkey detrusor by beta-adrenoceptor activation is mediated via the beta3-subtype.

Adrenergic beta-Agonists↗
PubMed2004

Myoclonus and metabolic alkalosis from licorice in antacid.

A 90-year-old woman with hypertension developed metabolic alkalosis and myoclonus. Her medications included diltiazem hydrochloride, benidipine hydrochloride, kallidinogenase, procaterol hydrochloride, sennoside, dihydrocodeine phosphate, and KM powder antacid that contained 354 mg of licorice and 900 mg of sodium bicarbonate per 3.9 g of powder. Endocrinological studies showed slightly reduced plasma renin activity and normal plasma aldosterone concentration. A provisional diagnosis of licorice-induced metabolic alkalosis was established and the patient was successfully treated after correction of serum pH and cessation of the medications. Licorice-induced metabolic alkalosis must be considered in the differential diagnosis of myoclonus.

Aged↗
PubMed2000

[Levofloxacin-induced eosinophilic pneumonia complicated by bronchial asthma].

A 76-year-old woman who had complained of cough and productive sputum since mid-January, 1999, was admitted to our hospital with fever and dyspnea on February 4, 1999. She had been treated with levofloxacin at an outpatient clinic. On admission, she had orthopnea, and auscultation revealed coarse crackles and wheeze in the bilateral lung fields. Chest x-ray and CT films showed non-segmental infiltration in bilateral lung fields. Laboratory data revealed eosinophilia in peripheral blood (= 24%) and sputum (= 10%), airflow limitation, hypoxemia (PaO2: 46 Torr), and increased airway responsiveness to methacholine (Dmin: 0.127 units). A bronchoalveolar lavage (BAL) fluid showed increased total cells and a 55% increase in eosinophils, and CD4/CD8 ratio was decreased to 0.8. In addition, IL-5 was increased in BAL fluid. Transbronchial lung biopsy specimens revealed infiltrations of eosinophils in the alveolar and interstitial compartments. Histological features of the bronchial biopsy specimens included increased eosinophils in the submucosa and goblet cell metaplasia. The woman was diagnosed with eosinophilic pneumonia complicated by bronchial asthma. She was given theophylline, pranlukast hydrate, and an inhaled beta 2 receptor agonist (procaterol hydrochloride), and pre-admission drugs including Levofloxacin were discontinued. Her symptoms were improved, peak expiratory flow rate and PaO2 increased, airway responsiveness to methacholine decreased (Dmin: 0.615 units), and radiographic abnormalities disappeared without steroid therapy. A leukocyte migration test for levofloxacin was weakly positive. An environmental provocation test in the patient's home gave negative results. A challenge test for levofloxacin was not performed due to a lack of informed consent. Based on these findings, we diagnosed this case as levofloxacin-induced lung injury manifesting as eosinophilic pneumonia complicated by bronchial asthma. Levofloxacin should be added to the list of agents that can produce eosinophilic pneumonia.

Aged↗
PubMed2000

Existence of a beta3-adrenoceptro and its functional role in the human ureter.

PURPOSE: We tried to determine the beta-adrenoceptor (AR) subtypes distributed in the human ureter and to clarify their functional role in ureteral relaxation. MATERIALS AND METHODS: 1) Effects of beta-AR agonists on either spontaneous or KCl-induced contractions of the human ureter and the antagonism by beta-AR antagonists on isoprenaline (a non-selective beta-AR agonist)-induced effects were evaluated in vitro. 2) Displacement by beta-AR antagonists of [3H]-dihydroalprenolol binding to a membrane preparation derived from human ureteral smooth muscle was evaluated. 3) A reverse transcription polymerase chain reaction assay was performed to determine the expression of the mRNA for beta1-, beta2- and beta3-ARs in human ureteral smooth muscle. RESULTS: 1) Isoprenaline and procaterol (a beta2-AR agonist) concentration-dependently suppressed both spontaneous and KCl-induced contractions of the human ureter. The beta3-AR agonists, CGP-12177A and CL-316243, also suppressed these ureteral contractions, but dobutamine (a beta1-AR agonist) had little relaxing effect. The rank order of relaxing potency for the catecholamines was isoprenaline > adrenaline > noradrenaline. ICI-118,551 (a beta2-AR antagonist) only partially antagonized the isoprenaline-induced relaxation. 2) Propranolol (a non-selective beta-AR antagonist) and ICI-118,551 concentration-dependently displaced [3H]-dihydroalprenolol binding to the membrane with Ki values of 1.5 x 10-9 M and 6.3 x 10-9 M, respectively, while metoprolol (a beta1-AR antagonist) was less effective in this assay. 3) beta1-, beta2- and beta3-AR mRNAs were all expressed in human ureteral smooth muscle. CONCLUSION: The present results provide the first evidence that the beta3-AR subtype is distributed in human ureteral smooth muscle and that it, and beta2-AR, mediate the ureteral relaxation induced by adrenergic stimulation.

Adult↗
PubMed1990

Subtype-selective modulation of human beta 1- and beta 2-adrenoceptor function by beta-adrenoceptor agonists and antagonists.

In healthy volunteers a 14-day treatment with the selective beta 1-adrenoceptor agonist xamoterol (2 x 200 mg/day) desensitized beta 1-adrenoceptor-mediated physiological effects, but did not affect beta 2-adrenoceptor-mediated effects; in contrast, a 9-day treatment with the selective beta 2-adrenoceptor agonist procaterol (2 x 50 micrograms/day) desensitized beta 1-adrenoceptor-mediated physiological effects, but did not affect beta 1-adrenoceptor-mediated effects suggesting that in general in man long-term treatment with beta-adrenoceptor agonists down-regulates beta-adrenoceptors, but in a beta-adrenoceptor subtype-selective manner. Similarly, in patients undergoing coronary artery bypass grafting chronic treatment with different beta-adrenoceptor antagonists without intrinsic sympathomimetic activity subtype-selectively up-regulated beta-adrenoceptors: non-selective antagonists (propranolol, sotalol) increased both cardiac beta 1- and cardiac, saphenous vein and lymphocyte beta 2-adrenoceptors, whereas beta 1-selective antagonists (metoprolol, atenolol, bisoprolol) increased only cardiac beta 1-, but not cardiac, saphenous vein or lymphocyte beta 2-adrenoceptors. Such a subtype-selective modulation of human beta 1- and beta 2-adrenoceptors should be taken into consideration when treating patients chronically with beta-adrenoceptor agonists and/or antagonists.

Adrenergic beta-Agonists↗
PubMed1991

[The clinical benefit of high dose inhalation therapy with beclomethasone dipropionate for patients with chronic bronchial asthma].

Conventional doses of aerosolized beclomethasone dipropionate (BDP) of up to 400 micrograms/day by inhalation has often failed to normalize the pulmonary function of chronic adult patients. Therefore it may be necessary to administer the individual maximum dose of BDP to reduce bronchial inflammation. In 13 patients (2 males and 11 females, mean age 49.2 +/- 3.7 years old) with chronic asthma whose minimum %PEFRs were lower than 80% under treatment with conventional doses of BDP, the clinical benefit of high dose inhalation therapy with BDP was studied for four consecutive weeks by comparing % peak expiratory flow rate (%PEFR) measured four times a day both before and 10 minutes after inhaled procaterol (PCR) in a cross-over fashion. Mean morning %PEFRs before inhaled PCR during the first two weeks with a lower dose of BDP (419 +/- 24 micrograms/day) and during the following two weeks with a higher dose of BDP (904 +/- 55 micrograms/day) were 60.6 +/- 3.1% and 77.5 +/- 4.1%, respectively (p less than 0.01). Average increases in %PEFR during the higher dose period before and after inhaled PCR were 12.1% and 12.4%, respectively, which was observed by the end of the first week after the start of higher dose of BDP in 12 out of 13 patients. Since there were no adverse reactions such as hoarseness, oral thrush and candidiasis during the period with higher doses of BDP, it was concluded that we should promptly employ higher doses of BDP in patients who did not respond satisfactorily to conventional doses of BDP.

Administration, Inhalation↗
PubMed1990

[Effect of a spacer device used with metered dose inhaler].

Metered dose inhaler (MDI) is widely used in treatment of bronchial asthma. But adequate efficacy is not obtained if the patients use an improper technique of inhalation. The spacer device was designed to reduce such inhalation errors. Three types of spacers (pear type, tube type, paper spacer) were studied to confirm their usefulness in bronchial asthma. Bronchodilating effect of procaterol (10 micrograms/puff X 2) in conventional MDI or MDI with a spacer was evaluated. There were no significant difference in the effect on the pulmonary function after single inhalation of MDI with or without a spacer for 60 minutes. In regular use of MDI with a spacer for two weeks, PEFR and FEV1.0 were slightly improved. These results suggest that effect of MDI with a spacer may be more effective than MDI alone in regular use.

Administration, Inhalation↗
PubMed1989

Differential regulation of fat cell beta-2 and beta-1 adrenoceptors by endogenous catecholamines in dog.

The effects of long-term endogenous catecholamine exposure on the regulation of leukocyte and adipocyte beta adrenoceptor subtypes were studied through an experimental model of chronic neurogenic hypertension in the dog. Chronic sinoaortic denervation (SAD) is associated with a significant increase in plasma catecholamine levels, a reduction in the total beta adrenoceptor number of the leukocytes (52%) as well as of the omental adipocytes (59%). Using highly selective beta antagonists (bisoprolol for beta-1; ICI 118,551 for beta-2 adrenoceptors) we demonstrate that the normal dog fat cell possess both beta-2 and beta-1 adrenoceptors in proportions of 67 and 33%, respectively. SAD-induced catecholamine enhancement promotes a strong reduction of beta-2 (but not beta-1) adrenoceptor number (from 237 +/- 28 to 52 +/- 13 fmol/mg of protein) leading to a new relative distribution in fat cell membranes: 36% for beta-2 and 64% for beta-1 adrenoceptors. Such a different regulation provokes major consequences in the associated-biological effect on adipocytes when evaluating the lipolytic process. Lipolysis induced by epinephrine or isoproterenol (two mixed agonists) is weakly but significantly reduced whereas lipolysis induced by procaterol (a highly selective beta-2 agonist) is strongly reduced. These data fit with the results of the binding studies and demonstrate the loss in beta-2 adrenoceptor number and efficiency in SAD dogs. The present study demonstrates a differential regulation of beta adrenoceptors: beta-2 but not beta-1 adrenoceptors are decreased by long-term exposure to high plasma levels of endogenous catecholamines in the dog.

Adipose Tissue↗
PubMed1989

[New methods for measurement of peripheral airway resistance].

We have developed two new methods to evaluate the peripheral resistance of the lung. The first is a method for continuous measurement of the frequency dependence of dynamic compliance (Cdyn, f.d.) and pulmonary resistance (RL) from a single-breath cycle by Fourier-series analysis. In this method, we have found that procaterol my first dilate the central airway and then gradually dilate the peripheral airway in bronchial asthma. The second is a method for the direct measurement of peripheral resistance by the anterograde catheter system using a catheter tip micromanometer. The catheter tip was inserted into the 3 mm diameter small airway anterogradely and intrabronchial pressure was measured simultaneously with transpulmonary pressure and mouth flow. We have found that the values of peripheral resistance in patients with COPD are four to seven times higher than that of normal subjects. These results suggest that the behavior of the peripheral and central airway may differ between patients and that the peripheral airway may be important to examine the pathogenesis of COPD.

Adult↗
PubMed1989

[Inhibitory effect of bronchodilators on cholinergic and peptidergic contractions of guinea-pig isolated bronchial muscle].

The effect of bronchodilators on neurogenic contractions was studied using isolated bronchial strip-chain preparations from guinea-pigs. Electrical field stimulation (8 Hz, 0.5 msec, 30 V, 40 pulses) evoked a biphasic contraction of the bronchial muscle, consisting of an initial phasic component followed by a sustained one which was mediated by cholinergic and peptidergic nerve stimulations, respectively. All the beta-stimulants and xanthines tested caused a concentration-dependent inhibition in the height of the electrically-induced biphasic contraction, with the following order of potency: procaterol greater than fenoterol greater than salbutamol greater than isoproterenol greater than adrenaline greater than enprofylline greater than aminophylline greater than ephedrine. Ipratropium bromide selectively inhibited the electrically-induced cholinergic contraction. Submaximal contractions of the bronchial muscle evoked by exogenous substance P (2 X 10(-7)M) were less potently inhibited by these drugs than those evoked by exogenous acetylcholine (2 X 10(-6)M). These results indicate that in isolated guinea-pig bronchial muscle, bronchodilators may inhibit cholinergic and peptidergic neurotransmissions mainly by postsynaptic depression of the responsiveness and partly by presynaptic reduction of the transmitter release.

Animals↗
PubMed1985

Comparison of beta-adrenoceptor populations in cat and guinea-pig left atria.

The subtypes of beta-adrenoceptor present in left atrial preparations from the guinea-pig and cat have been assessed using both responses obtained in organ bath experiments and radioligand binding studies. From the positive inotropic responses to procaterol, the pKB values for practolol using a variety of agonists, and from displacement of [125I]cyanopindolol from left atrial membrane homogenates by the selective beta 1- and beta 2-adrenoceptor antagonists L643,717-01J10 and ICI 118,551, it was concluded that guinea-pig left atria possess only beta 1-adrenoceptors, whilst cat left atria possess both beta 1- and beta 2-adrenoceptor subtypes.

Adrenergic beta-Antagonists↗
PubMed1985

[Influence of arachidonic acid metabolic inhibitors upon uterine contractions].

The stimulating action of uterine contractions of cyclooxygenase products and 5-lipoxygenase products in an arachidonic acid cascade and the role of the inhibitors of both pathways have recently been the subject of much attention. We studied the influences of these drugs using the myometriums of pregnant rats. The inhibitory effects on pregnant uterine contractions (in vitro) were in the order beta 2-stimulants (procaterol, pirbuterol) greater than AA-861 greater than flurbiprofen greater than indomethacin greater than BW-755C. The inhibitory potency was reinforced by concurrent administration of AA-861 and flurbiprofen. Stimulation of the uterine contractions by Leukotriene (LT) was LTD4 greater than LTC4, and also the inhibition of the LT strain was AA-861 greater than flurbiprofen. The stimulation of PGE1 analog (ONO-802) revealed the reaction of LT + AA-861 (-) and LT + flurbiprofen (+/-). As to the changes in c-AMP and c-GMP in the bath medium before and after the administration of each drug, the change in the administration of the LT strain was slight, and an increase in c-AMP and a decrease of c-GMP were noted following the administration of contraction inhibitory substances. Its variation ratios were noted, in the order: increase in c-AMP of AA-861 + flurbiprofen greater than pirbuterol AA-861 greater than BW-755C, and decrease in c-GMP of pirbuterol greater than AA-861 + flurbiprofen greater than A-861 greater than BW-755C.

Adrenergic beta-Agonists↗