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PubMed1988

Relaxant and beta 2-adrenoceptor blocking activities of labetalol, dilevalol, amosulalol and KF-4317 on the rat isolated aorta.

The KCl-contracted rat aorta is relaxed by labetalol, dilevalol, amosulalol and KF-4317. These relaxations are not reversed by ICI 118,551 at 10(-6) M and, therefore, are not due to beta-adrenoceptor agonism. At 10(-7) M, labetalol, dilevalol, amosulalol and KF-4317 were beta 2-adrenoceptor antagonists as they inhibited the relaxant responses of rat aorta to procaterol.

Adrenergic beta-Agonists↗
PubMed2003

Functional and molecular characterization of beta-adrenoceptors in the internal anal sphincter.

The purpose of the present study was to characterize different beta-adrenoceptors (beta-ARs) and determine their role in the spontaneously tonic smooth muscle of the internal anal sphincter (IAS). The beta-AR subtypes in the opossum IAS were investigated by functional in vitro, radioligand binding, Western blot, and reverse transcription-polymerase chain reaction (RT-PCR) studies. ZD 7114 [(S)-4-[2-hydroxy-3-phenoxypropylaminoethoxy]-N-(2-methoxyethyl)phenoxyacetamide], a selective beta(3)-AR agonist, caused a potent and concentration-dependent relaxation of the IAS smooth muscle that was antagonized by the beta(3)-AR antagonist SR 59230A [1-(2-ethylphenoxy)-3-[[(1S)-1,2,3,4-tetrahydro-1-naphthalenyl]amino]-(2S)-2-propanol hydrochloride]. Conversely, the IAS smooth muscle relaxation caused by beta(1)- and beta(2)-AR agonists (xamoterol and procaterol, respectively) was selectively antagonized by their respective antagonists CGP 20712 [(+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2-yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate salt] and ICI 118551. Saturation binding of [(125)I]iodocyanopindolol to beta-AR subtypes revealed the presence of a high-affinity site (K(d1) = 96.4 +/- 8.7 pM; B(max1) = 12.5 +/- 0.6 fmol/mg protein) and a low-affinity site (K(d2) = 1.96 +/- 1.7 nM; B(max2) = 58.7 +/- 4.3 fmol/mg protein). Competition binding with selective beta-AR antagonists revealed that the high-affinity site correspond to beta(1)/beta(2)-AR and the low affinity site to beta(3)-AR. Receptor binding data suggest the predominant presence of beta(3)-AR over beta(1)/beta(2)-AR. Western blot studies identified beta(1)-, beta(2)-, and beta(3)-AR subtypes. The presence of beta(1)-, beta(2)-, and beta(3)-ARs was further demonstrated by mRNA analysis using RT-PCR. The studies demonstrate a comprehensive functional and molecular characterization of beta(1)-, beta(2)-, and beta(3)-ARs in IAS smooth muscle. These studies may have important implications in anorectal and other gastrointestinal motility disorders.

Adrenergic beta-Agonists↗
PubMed1997

Role of beta1- and beta3-adrenoceptors in the regulation of lipolysis and thermogenesis in rat brown adipocytes.

To evaluate the physiological functions of beta1-, beta2-, and beta3-adrenoceptors (ARs) in brown adipose tissue, the lipolytic and respiratory effects of various adrenergic agonists and antagonists were studied in rat brown adipocytes. The beta-agonists stimulated both lipolysis and respiration (8-10 times above basal levels), with the following order of potency (concentration eliciting 50% of maximum response): CL-316243 (beta3) > BRL-37344 (beta3) > isoproterenol (mainly beta1/beta2) > norepinephrine (NE; mainly beta1/beta2) > epinephrine (mainly beta1/beta2) >> dobutamine (beta1) >> procaterol (beta2). Schild plot coefficients of competitive inhibition experiments using ICI-89406 (beta1 antagonist) revealed that more than one type of receptor mediates NE action. It is concluded from our results that 1) NE, at low plasma levels (1-25 nM), stimulates lipolysis and respiration mainly through beta1-ARs, 2) NE, at higher levels, stimulates lipolysis and respiration via both beta1- and beta3-ARs, 3) beta2-ARs play only a minor role, and 4) beta3-ARs may represent the physiological receptors for the high NE concentrations in the synaptic cleft, where the high-affinity beta1-ARs are presumably desensitized. It is also suggested that lipolysis represents the flux-generating step regulating mitochondrial respiration.

Adipocytes↗
PubMed2005

Differential effects of short-acting beta2-agonists on human granulocyte functions.

BACKGROUND: beta2-Adrenergic agonists play a pivotal role in the management of bronchial asthma. Although the major effect of short-acting beta2-agonists on the airway is relaxation of smooth muscles, they may also have several effects on surrounding immunomodulatory cells. METHODS: We examined whether widely used short-acting beta2-agonists differ in their ability to modulate granulocyte functions, such as superoxide anion (O2-) production and degranulation. RESULTS: Procaterol (PC), a full agonist, significantly inhibited both O2- production by granulocytes (neutrophils and eosinophils) and their degranulation at the clinically relevant concentrations, whereas salbutamol and tulobuterol (partial agonists) showed smaller effects. PC inhibited N-formyl methionyl-leucyl-phenylalanine-induced O2- production and peroxidase release, but failed to inhibit responses induced by phorbol 12-myristate 13-acetate and/or opsonized zymosan. Exposure to 5 x 10(-8)M PC for 120 min resulted in approximately 50% inhibition of O2- production and degranulation of neutrophils. The effects of beta2-agonists were more obvious in neutrophils than in eosinophils. A selective beta2-receptor antagonist, ICI-118551, reversed the inhibitory effect of beta2-agonists (PC, salbutamol, tulobuterol B) on N-formyl methionyl-leucyl-phenylalanine-induced O2- production. CONCLUSIONS: These results suggest that beta2-agonists had an inhibitory effect on granulocyte functions, mainly mediated viareceptors and their efficacy. Our observations support that beta2-agonists with a rapid onset of action and high intrinsic efficacy (short-acting and full agonists) may be optimal for the rescue therapy against acute asthma attack and sedation of its airway inflammation in an early phase.

Adrenergic beta-Agonists↗
PubMed1996

Angiotensin-converting enzyme inhibitor and danazol increase sensitivity of cough reflex in female guinea pigs.

To examine the mechanisms of an angiotensin-converting enzyme (ACE) inhibitor-induced cough in perimenopausal and postmenopausal women, cough responses to aerosols of capsaicin and citric acid were examined in four groups of female guinea pigs treated orally with danazol (D) (an agent decreasing plasma estrogen levels), cilazapril (C) (an inhibitor of ACE), both danazol and cilazapril (C+D), or without either drug (control group) for 4 to 5 wk. Capsaicin caused dose-dependent increases in the number of coughs in all four groups. C or D alone shifted dose-response curves to capsaicin (from 10(-7) M to 10(-3) M) to lower concentrations compared with the control, and C+D further shifted them. Likewise, the number of coughs induced by citric acid (3 x 10(-1) M; 2 min) was highest in animals treated with C+D and significantly higher in animals treated with C or D than in the control group. Aerosols of a selective substance P (SP) receptor antagonist FK 888 (10(-5) M; 2 min) inhibited capsaicin-induced cough in all four groups, and dose-response curves to capsaicin did not differ significantly at any concentrations among the four groups in the presence of FK 888 (p > 0.10). D decreased cyclic AMP levels in the trachea, irrespective of the combination of C. A beta 2-adrenoceptor agonist, procaterol, which is thought to inhibit SP release by elevation of cyclic AMP in sensory nerves, dose-dependently inhibited the number of coughs induced by capsaicin (10(-3) M) in animals treated with D. The present study suggests that SP is a common mechanism mediating increases in the sensitivity of cough reflex induced by both ACE inhibition and a decrease in plasma estrogen levels, and the additive effects of the two events may explain the high incidence of cough during ACE inhibitor therapy in perimenopausal and postmenopausal women.

Adrenergic beta-Agonists↗
PubMed1989

Heterogeneity of beta-adrenoceptor in canine veins: comparison among the facial, portal and saphenous veins.

A study was made on the characteristics of beta-adrenoceptors in the isolated canine facial, portal and saphenous veins. Ring segments of the facial and saphenous veins and longitudinal strips of the portal vein were suspended in tissue baths containing Krebs solution oxygenated and maintained at 37 degrees C. They were moderately contracted with prostaglandin F2 alpha before examining their relaxation responses. The facial and saphenous veins fully relaxed to isoproterenol, while the portal vein relaxed to a small extent (20% of maximum relaxation) even in the presence of an alpha-adrenoceptor blockade. In contrast, both forskolin, a direct activator of adenylate cyclase, and membrane-permeable dibutyryl cyclic AMP similarly relaxed all the veins studied. Thus, the reduction of coupling between beta-adrenoceptors and the adenylate cyclase system may be involved in the decreased responsiveness of the portal vein to beta-adrenoceptor agonists. In addition, analyses of beta-adrenoceptor agonism and antagonism, using selective (beta 1: T-1583, beta 2: procaterol) and non-selective (isoproterenol) agonists as well as selective (beta 1: atenolol, beta 2: ICI 118,551) and non-selective (propranolol) antagonists, confirmed that beta-adrenoceptors in the canine facial vein are not homogeneous, with the beta 1-subtype predominating over the beta 2-subtype, and that the canine saphenous vein has a homogeneous population of the beta 2-subtype, as reported in the other species.

Adenylyl Cyclases↗
PubMed1990

Pharmacological analysis of positive chrono- and inotropic responses to denopamine (TA-064) in dog cross-circulated atrial and ventricular preparations.

Positive chrono- and inotropic responses to denopamine (TA-064, (-)-(R)-1-(p-hydroxyphenyl)-2-[(3,4-dimethoxyphenethyl)amino]ethanol), a new and orally active cardiotonic agent, were investigated in the canine isolated right atrial or left ventricular preparation which was cross-circulated with blood from another support dog. Denopamine dose-dependently increased the sinus rate, right atrial and left ventricular contractile force. Denopamine was one to two orders of magnitude less potent than isoproterenol. The positive chrono- and inotropic effects of denopamine in isolated, blood-perfused right atria were dose-dependently inhibited by treatment with propranolol and atenolol. The effects of denopamine were only slightly attenuated by ICI 118,551 in doses which completely suppressed the positive chrono- and inotropic effects of procaterol. The increases in sinus rate and atrial contractility induced by denopamine were partially but significantly attenuated by treatment with imipramine in a dose which suppressed the effects of tyramine and potentiated the effects of norepinephrine. These results indicate that denopamine is a highly selective beta-1 adrenoceptor agonist in isolated, blood-perfused dog heart preparations, and they also suggest a mild catecholamine-releasing activity through tyramine-like action in isolated right atria.

Adrenergic beta-Antagonists↗
PubMed2006

Safety and usefulness of a novel eMotion electric mesh nebulizer in children with asthma.

BACKGROUND: A new electronic mesh nebulizer, eMotion is known to have higher performance compared to conventional nebulizers. However, there are some concerns about whether too much delivered dose might cause side effects with higher frequency. METHODS: To evaluate the safety and usefulness of the nebulizer, we measured changes in heart rates and lung functions of 73 asthmatic children when they inhaled 1 microg/kg of procaterol with eMotion or a conventional nebulizer, Junior BOY. RESULTS: In 34 children with mild asthma exacerbation, physical findings, lung function and transcutaneous oxygen saturation levels were improved after inhalation using both nebulizers. No adverse effects including significant increase of heart rate were found. Improvements in the rates of the parameters were comparable. When response to beta2-agonist inhalation was checked in 39 children in stable condition, similar degrees of improvement in lung function were observed, and heart rates did not change after inhalation with either nebulizers. CONCLUSIONS: Safety and efficacy was comparable between eMotion and a conventional nebulizer when it was used to administer beta2-agonists in asthmatic children. However, from the fact that eMotion needs only 3-4 minutes to inhale 2 mL solution, eMotion could be more useful for most children who usually do not prefer longer inhalation time with conventional compressor nebulizers.

Administration, Inhalation↗
PubMedDate not supplied

Selective beta2-adrenoceptor agonist enhances sensitivity to cisplatin in non-small cell lung cancer cell line.

Cisplatin is a key drug in chemotherapy for lung cancer. It has been reported that intracellular accumulation of cisplatin is an important step as a determinant for resistance to cisplatin, which may be modulated by Na+, K+-ATPase activity. And it has been reported that isoproterenol, a beta-adrenoceptor agonist, enhances sensitivity to cisplatin in non-small cell lung cancer (NSCLC) cell lines. In this study, the effects of the selective beta1, beta2, and beta3-adrenoceptor agonists on membrane Na+, K+-ATPase activity and sensitivity to cisplatin were evaluated using human non-small cell lung cancer cell line. In the NSCLC cell line, sensitivity to cisplatin was improved by treatment with procaterol, a selective beta2-adrenoceptor agonist. Na+, K+-ATPase was activated and intracellular accumulation of cisplatin increased with the treatment. However, beta1 or beta3-adrenoceptor agonist did not modulate sensitivity to cisplatin or Na+, K+-ATPase activity. These results suggest that beta2-adrenoceptor may be one of the determinants for sensitivity to cisplatin in NSCLC. Exogenous beta2-adrenoceptor agonists may improve the antitumor effect of chemotherapy involving cisplatin.

Adrenergic beta-2 Receptor Agonists↗
PubMed1999

Regional and gender variations in adipose tissue lipolysis in response to weight loss.

Catecholamine-induced lipolysis was investigated in 32 obese subjects (14 men and 18 premenopausal women), aged 36-50 years, whose body mass index ranged from 30 to 42 kg/m(2). Isolated subcutaneous (subc) abdominal and femoral adipocytes were studied before and after a 15-week weight reducing program, during which mean body weight loss averaged 9 vs. 10 kg in women and men, respectively (P < 0.0001). Participants were re-examined when they were weight-stable. Fat cell weight decreased by about 15;-20% in both depots (P values ranging from 0.01 to 0.05). Epinephrine (mixed alpha2-/beta-adrenoceptor (AR) agonist) induced antilipolysis at low concentrations and a net lipolytic response at higher doses, irrespective of subjects' fatness and anatomic location of fat. Basal lipolysis, maximal lipolytic responses to isoprenaline (beta-AR agonist), dobutamine and procaterol (beta1- and beta2-AR agonists, respectively) as well as maximal antilipolytic effects of epinephrine or UK-14304 (alpha2-AR agonist) were similar before and after weight reduction. However, both beta- and beta2-AR lipolytic sensitivities and the beta-AR density were increased in both genders after weight reduction, this effect being more marked in subc abdominal than in femoral adipocytes (P values ranging from 0.001 to 0.05). The alpha2-AR antilipolytic sensitivity was reduced in adipose cells from both regions in women, but only in subc abdominal adipocytes in men (P < 0.05), although the alpha2-AR density remained unchanged after weight reduction. In conclusion, a moderate weight loss leads to a higher adipose cell lipolytic efficiency which is associated with changes at receptor levels (mainly an increased beta2- and a decreased alpha2-AR sensitivities), in both genders.

Adenosine Deaminase↗
PubMed1986

Oral beta 2-selective adrenergic bronchodilators.

Oral beta 2-agonists (carbuterol, pirbuterol, procaterol, bitolterol, clenbuterol) are drugs widely used as bronchodilators. The efficacy and selectivity of bronchodilators drugs depend on their intrinsic pharmacological properties and on the route of administration. The characteristics of the oral route are easy usage, precise dosage and assured effects. Consequently, disadvantages (delayed onset of action, more frequent side-effects) and the indications, (patients with severe chronic airways obstruction, nocturnal asthmatic attacks, and children and elderly subjects) are clearly evident. The most recent beta 2-agonists have an efficient and prolonged bronchodilating action with well-known side-effects. In order to control drug efficiency in a large population and identify type and degree of adverse reactions, a post-marketing surveillance study was programmed for clenbuterol. The results available confirms that long-term treatment with oral clenbuterol is an effective and safe therapeutical approach. During long-term treatment, tachyphylaxis (a diminished responsiveness) develops. This complex biological phenomenon can be studied, in several ways i.e. functional response of target-organ, appropriate biochemical-metabolical indices, and functional evaluation of the cellular beta-receptors in vitro. Also in the light of evaluation of serum levels of cyclic nucleotides (cyclic adenosine and guanosine monophosphates) it appears that the clinical importance of tachyphylaxis is mild and that chronic therapy with beta 2-agonists is safe and effective when used in selected patients.

Administration, Oral↗
PubMed1995

[Effects of a beta 2-agonist, sodium cromoglycate, and an anticholinergic agent on hyperventilation-induced bronchoconstriction in sensitized rabbits].

Hyperventilation can induce bronchoconstriction in ovalbumin-sensitized rabbits. To investigate the roles of the beta-receptor parasympathetic nervous system and of chemical mediators in hyperventilation-induced bronchoconstriction (HIB), the effects of a beta 2-agonist, of sodium cromoglycate, and of an anticholinergic agent on HIB were studied. Rabbits were divided to four groups and treated as follows. Group 1: Control (n = 7, 0.9% saline); Group 2: Procaterol (n = 4, 50 micrograms/l); Group 3: Sodium cromoglycate (n = 4, 10 mg/ml); and Group 4: Ipratropium bromide (n = 6, 1 mg/ml). Each drug was inhaled for 1 min via an ultrasonic nebulizer. Then, for the eucapnic hyperventilation challenge, sensitized rabbits were mechanically hyperventilated for 15 min (120 breaths/min, tidal volume = 7 ml/kg) with dry air containing 5% CO2 at room temperature. Total lung resistance and dynamic compliance were measured before, and 0, 5, 15, and 30 min after hyperventilation. The mean percent change in resistance measured 5 min after the hyperventilation was +49% in group 1, -6% in group 2, +23% in group 3, and +1% in group 4. The changes in groups 2 and 4 were significantly less than in group 1 (p < 0.05). In conclusion, HIB is mainly caused by bronchial smooth muscle constriction, and chemical mediators and the parasympathetic nervous system may play important roles in the development of HIB in sensitized rabbits.

Acetylcholine↗
PubMed1996

[Anti-allergic effects of beta-adrenoceptor agonists in the clinical pharmacological studies].

Beta-adrenoceptor agonists have several pharmacological actions in the lung which affect airway function. They have a direct relaxant effect on human bronchial smooth muscle and several additional properties, including attenuation of mast cell mediater release, reduction in airway microvascular leakage, and inhibition of cholinergic neurotransmission within the airway, in vitro. However, direct evidence in vivo for any anti-inflammatory effects of beta-adrenocepter agonists is limited. We reported that beta-agonists (procaterol, salmeterol) inhibited significantly I. A. R. and L. A. R. Salmeterol also reduced urinary secretion of LTE4. It is suggested that beta-agonists have some of anti-allergic effects in the clinical pharmacological study. From recent clinical studies, it is recommended on demand use more than regular use of inhaled beta-agonists.

Adrenergic beta-Agonists↗
PubMed1996

[Long-term effects of inhaled beta 2-agonists on bronchial hyperresponsiveness in asthmatics].

We examined the effects of two year's treatment of three inhaled beta 2-agonists (beta 2), such as salbutamol (S), procaterol (P) and fenoterol (F) on acetylcholine induced bronchial hyperresponsiveness (BHR) in mild approximately moderate asthmatics. When symptomatic use of beta 2 were less than 6 puffs/day, BHR was improved significantly with both S and P but was not with F. When more than 6 puffs/day, all three beta 2 did not show the improvement of BHR. Without the effect of corticosteroids, BHR was improved with S, and was partially improved with P in case of only less than 6 puffs/day, but was not improved with F unrelated to the inhaled puff number. Therefore, frequent use of beta 2 even if used only on demand was shown to worse BHR, asthmatics must be controlled to under the good condition of using beta 2 at least less than 6 puffs/day.

Administration, Oral↗
PubMed1996

[The clinical usefulness of the combined use of inhaled beta 2-agonist and inhaled steroid in asthma].

Treatment with inhaled steroid has become increasingly important in asthma. However there are also many patients with asthma whose symptoms are uncontrolled by beclomethasone dipropionate (BDP) alone. For these patients we have tried the regular use of inhaled procaterol or inhaled fenoterol with BDP, and some of these patients have got good control. Recent studies show that, in patients whose asthma is inadequately controlled with BDP, better control can be achieved by adding inhaled long-acting beta 2-agonist rather than by doubling the dose of BDP. In the near future inhaled long-acting beta 2-agonist will be possible for clinical use in our country, and the combined use of it and BDP as preventive therapy will be the mainstay of treatment for patients with moderate-to-severe asthma.

Adrenergic beta-Agonists↗
PubMed2001

Bronchodilators for the prevention and treatment of chronic lung disease in preterm infants.

BACKGROUND: Chronic lung disease (CLD) occurs frequently in preterm infants (< 37 weeks gestational age) and has a multifactorial etiology. Bronchodilators have the potential effect of dilating small airways with muscle hypertrophy. Increase in compliance and tidal volume and decrease in pulmonary resistance have been documented with use of bronchodilators in short term studies of pulmonary mechanics in infants with CLD. Therefore it is possible that bronchodilators might have a role in the prevention and treatment of CLD. OBJECTIVES: To evaluate the effect of bronchodilators, given prophylactically or as treatment for chronic lung disease, on mortality and other complications of preterm births. SEARCH STRATEGY: The search strategy used to identify studies was according to the guidelines of the Cochrane Neonatal Review Group. Searches were made of MEDLINE 1966 to December 2000, EMBASE 1980 to January 2001, CINAHL 1982 to December 2000, the Cochrane Library Issue 1, 2001, personal files and reference lists of identified trials. The following terms were used: bronchopulmonary dysplasia, chronic lung disease, bronchodilator agents, adrenergic agents, anticholinergic agents, albuterol, aminophylline, atropine, caffeine, clenbuterol, cromakalim, ephedrine, epinephrine, fenoterol, hexoprenaline, ipratropium, isoetharine, isoproterenol, orciprenaline, procaterol, terbutaline, theophylline, tretoquinol. LIMITS: newborn, infant; human, clinical trial or controlled clinical trial, meta analysis, multicenter study or randomised controlled trial. No language restrictions were applied. SELECTION CRITERIA: Randomised controlled clinical trials involving preterm infants. Initiation of bronchodilator therapy had to occur within two weeks of birth for prevention of CLD. For treatment of CLD treatment should have been initiated before discharge from the neonatal unit. The intervention had to include the randomised administration of a bronchodilator either by nebulisation, metered dose inhaler with or without a spacer device, intravenously or orally, versus placebo or no intervention. Eligible studies had to include at least one of the following outcomes: mortality, CLD at 28 days or at 36 weeks corrected GA, number of days on oxygen, number of days on ventilator, patent ductus arteriosus (PDA), pulmonary interstitial emphysema (PIE), pneumothorax, any grade of intraventricular haemorrhage, necrotizing enterocolitis (NEC), sepsis and adverse effects of bronchodilators. DATA COLLECTION AND ANALYSIS: We used the standard method for the Cochrane Collaboration as described in the Cochrane Collaboration handbook. Two investigators (GN, AO) extracted and assessed all data for each study. Any disagreement was resolved by discussion. Relative risk (RR) and risk difference (RD) with 95% confidence intervals (CI) are reported for dichotomous outcomes and mean difference (WMD) for continuous data. MAIN RESULTS: One eligible study was found dealing with prevention of CLD; this study used salbutamol and enrolled 173 infants. No eligible studies were found dealing with treatment of CLD. Prophylaxis with salbutamol did not show a statistically significant difference in mortality [RR 1.08 (95% CI 0.50, 2.31); RD 0.01 (95% CI -0.09, 0.11)], CLD (mild, moderate or severe) [RR 1.03 (95% CI 0.78, 1.37); RD 0.02 (95% CI -0.13, 0.17)], need for iv dexamethasone [RR 0.77 (95% CI 0.49, 1.19); RD -0.08 (95% CI -0.22, 0.05)], respiratory infections [RR 0.61 (95% CI 0.27, 1.39); RD -0.06 (95% CI -0.16, 0.04)] or positive blood culture [RR 1.06 (95% CI 0.54, 2.06); RD 0.01 (95% CI -0.10, 0.12)]. There was no statistically significant difference in duration of ventilatory support [MD -1.63 days (95% CI -5.63, 2.37)], duration of oxygen supply [MD -2.82 days (95% CI -11.91, 6.27)] or age of weaning from respiratory support (defined as assisted ventilation or oxygen supplementation) [MD -2.87 days (95% CI -11.28, 5.54)]. No side effects due to salbutamol were commented on in this study. REVIEWER'S CONCLUSIONS: There are insufficient data to reliably assess the use of salbutamol for the prevention of CLD. Further clinical trials are necessary to assess the role of salbutamol or other bronchodilator agents in prophylaxis or treatment of CLD.

Bronchodilator Agents↗
PubMed1996

Regulation of the expression of the proenkephalin gene in cultured meningeal fibroblasts: opposite effects of alpha 1- and beta 2-adrenoceptors.

Meningeal fibroblasts express the proenkephalin gene during embryonal development but terminate the expression shortly before birth. When brought into primary culture at postnatal day 1, the fibroblasts again express the gene. Activation of protein kinase A reduces this expression and thus may contribute to its prenatal termination. Since the noradrenergic innervation of the meninges begins around the time of birth, it was investigated in the present study, how adrenergic agonists affected the levels of proenkephalin mRNA in cultured fibroblasts. The beta 2-adrenoceptor agonists salbutamol and procaterol increased the levels of endogenous cAMP and diminished the concentration of proenkephalin mRNA indicating that the cultured fibroblasts possessed this beta-subtype. In contrast, noradrenaline increased the level of proenkephalin mRNA in a concentration-dependent manner. This effect was independent of endogenous cAMP and was mediated by alpha 1-adrenoceptors. The data indicate that the noradrenergic innervation of the meninges at the time of birth is not responsible for the termination of the proenkephalin gene expression.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1988

Presynaptic beta 2-adrenoceptors on the sympathetic nerve fibres of the human saphenous vein: no evidence for involvement in adrenaline-mediated positive feedback loop regulating noradrenergic transmission.

Spirally cut strips of human saphenous veins preincubated with 3H-noradrenaline were superfused in the presence of corticosterone and, unless stated otherwise, of cocaine or desipramine. Tritium overflow was stimulated electrically (2 Hz). Adrenaline (in the presence of rauwolscine), isoprenaline and the preferential beta 2-adrenoceptor agonist procaterol concentration-dependently increased the electrically evoked tritium overflow. Prenalterol, a beta-adrenoceptor agonist with moderate preference for beta 1-adrenoceptors, was ineffective. The concentration-response curve of isoprenaline was shifted to the right by the nonselective beta-adrenoceptor antagonist propranolol and by the preferential beta 2-adrenoceptor antagonist ICI 118,551, but was not affected by the beta 1-selective antagonist atenolol. In experiments on strips preexposed to adrenaline 10 nmol/l (i.e. a concentration higher than that which normally occurs in vivo) for 32 min in the absence of cocaine or desipramine, the electrically evoked 3H overflow was not affected 12 and 44 min after withdrawal of adrenaline, irrespective of whether propranolol was absent or present in the superfusion fluid. In veins incubated with 3H-adrenaline, a considerable amount of the radioactivity was accumulated. During subsequent superfusion with 3H-adrenaline-free solution, electrical stimulation induced tritium overflow in a tetrodotoxin-sensitive manner. Propranolol failed to modify the evoked tritium overflow. It is concluded that the sympathetic nerve fibres of the human saphenous vein are endowed with facilitatory presynaptic beta 2-adrenoceptors. These receptors do not seem to play a substantial role in a local adrenaline (previously taken up)-mediated positive feedback loop regulating noradrenergic transmission, at least under the present in vitro conditions.

Adrenergic beta-Agonists↗