Disease relevance of PROCATEROL

• A placebo-controlled trial of procaterol: a new long-acting oral beta 2-agonist in bronchial asthma [1].
• BACKGROUND--To evaluate the effect of inhaled beta 2 adrenergic agonists on the sensitivity of airway cough receptors, the effect of inhaled procaterol on cough induced by aerosolised capsaicin, a stimulant of C fibres, was studied in patients with asthma or chronic bronchitis and in normal subjects [2].
• When coronary stenosis was absent, intracoronary infusion of procaterol (6.7 ng/min for 15 min) produced significant increases in LCX flow and myocardial segment shortening in the infused region without changes in global hemodynamics [3].
• Cardiac effects of beta-2 adrenoceptor stimulation with intracoronary procaterol in the absence and presence of regional myocardial ischemia in dogs [3].
• Procaterol (10 and 30 ng kg-1 min-1, i.v.) also produced hypotension but did not alter pressor responses to sympathetic nerve stimulation [4].

High impact information on PROCATEROL

• Procaterol decreased lymphocyte beta 2-adrenoceptor density and all beta 2-adrenoceptor-mediated in vivo effects but did not affect beta 1-adrenoceptor-mediated in vivo effects [5].
• Stimulation of beta2-adrenoceptors with the selective beta2 agonist procaterol caused a biphasic decrease in cell surface M2 muscarinic receptor number in human embryonic lung 299 cells when measured with the hydrophilic antagonist [3H]N-methylscopolamine [6].
• Procaterol-induced down-regulation of M2 receptors was fully blocked by N-[2-(methylamino)ethyl]-5'-isoquinoline-sulfonamide and 2-[1-(3-dimethylaminopropyl)-inol-3-yl]-3-(indol-3-yl)maleimide, implicating both of these kinases in the M2 muscarinic receptor down-regulation [6].
• 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 [7].
• Procaterol attenuated histamine-induced cough only at the concentrations effective to inhibit bronchoconstriction [8].

Chemical compound and disease context of PROCATEROL

• Inhaled procaterol versus salbutamol in bronchial asthma [9].
• Effect of inhaled procaterol hydrochloride in children with bronchial asthma, with particular reference to duration of effect [10].
• Preventive effect and duration of action of disodium cromoglycate and procaterol on exercise-induced asthma in asthmatic children [11].
• Therapeutic equivalence between procaterol hydrochloride dry powder inhaler (Meptin DPI) and procaterol hydrochloride metered-dose inhaler (Meptin MDI), the currently marketed formulation, was assessed in 16 patients with bronchial asthma [12].
• 18 children (6-15 years of age) with acute bronchial asthma attacks (FEV1 < 80% of the predicted value) received pirbuterol (N = 10) or procaterol (N = 8) by metered-dose inhaler, one puff every 5 minutes, for a total of five doses [13].

Biological context of PROCATEROL

• Changes in pulmonary function and cross-sectional area of trachea and bronchi in asthmatics following inhalation of procaterol hydrochloride and ipratropium bromide [14].
• Tremor, the most common side effect of ordinary doses of beta 2-agonists, was evaluated in a quantitative manner and compared to improvement in pulmonary function in respect to time of onset, duration, peak effect, and tachyphylaxis with procaterol in adults [15].
• To evaluate the bronchodilator effect of procaterol and the bronchoconstrictor effect of inhaled capsaicin, forced expiratory volume in one second (FEV1) was measured before and one minute after a capsaicin provocation test [2].
• In separate experiments procaterol (1 to 100 microgram./kg. intravenously) decreased mean blood pressure and increased heart rate in a dose dependent manner [16].
• Procaterol suffers major limitations since it strongly increases heart rate, immunoreactive insulin and glycaemia [17].

Anatomical context of PROCATEROL

• Compound 4 showed less potent beta-adrenoceptor stimulant activities than procaterol or terbutaline in an in vitro test using guinea pig tracheal muscle and right atrium [18].
• Relaxing actions of procaterol, a beta 2-adrenoceptor stimulant, on smooth muscle cells of the dog trachea [19].
• Low concentrations of procaterol (3 nM to 100 nM) relaxed KC1-contracted preparations of rat aorta and pulmonary artery from rat, rabbit and guinea-pig whereas high concentrations (greater than 1 microM) were required to relax preparations of the dog left circumflex coronary artery [20].
• The dissociation constant (KP value) for procaterol on beta 1-adrenoceptors was 4.9 microM (determined on dog coronary artery) and on beta 2-adrenoceptors was 0.008 microM (rabbit pulmonary artery) [20].
• RESULTS: 1) Isoprenaline and procaterol (a beta2-AR agonist) concentration-dependently suppressed both spontaneous and KCl-induced contractions of the human ureter [21].

Associations of PROCATEROL with other chemical compounds

• On the other hand, beta2-adrenergic receptor agonists, procaterol and alprenol, delayed barrier recovery and the beta2 receptor antagonist, ICI-118551, blocked the delay [22].
• The stainless-steel cannula-inserting method was used to observe vascular effects of mixed and selective beta adrenoceptor agonists, isoproterenol, procaterol and denopamine, on isolated, perfused rabbit common carotid arteries [23].
• Lesions of the locus coeruleus increased the responses to the beta 1-adrenoceptor agonists, prenalterol and dobutamine, but reduced the response to the beta 2-adrenoceptor agonists, salbutamol and procaterol [24].
• Metoprolol (10(-8) to 10(-7) M) inhibited only the dobutamine-induced vasorelaxation, but did not significantly influence the procaterol-induced response.(ABSTRACT TRUNCATED AT 250 WORDS)[25]
• 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 [26].

Gene context of PROCATEROL

• Neither dobutamine (beta1- and beta2-AR agonist) nor procaterol (beta2-AR agonist) produced any significant relaxation at concentrations up to 10(-5) M [27].
• The beta-agonists, procaterol, clenbuterol, fenoterol and terbutaline, inhibited TNF-alpha and IL-1 beta production in a concentration-dependent manner, whereas they had no effect on IL-8 production [28].
• In contrast to treatment with individual agonists, chronic dual agonist treatment suppresses procaterol-induced stimulation of ERK activity and stimulation of proliferation indicating that a cross-regulatory interaction occurs between the delta-OR and beta2-AR signalling systems in the cells under these conditions [29].
• Procaterol inhibits IL-1beta- and TNF-alpha-mediated epithelial cell eosinophil chemotactic activity [30].
• Procaterol inhibited the release of RANTES, GM-CSF and IL-8 in a dose-dependent fashion [30].

Analytical, diagnostic and therapeutic context of PROCATEROL

• Spirometry results indicated significant improvement in pulmonary function with both doses of procaterol compared with placebo (P less than 0.05) [1].
• This test was carried out both before and 30 minutes after treatment with procaterol or placebo [2].
• Inhaled procaterol significantly reduced in a dose-dependent manner the increment in TXB2 concentration in bronchoalveolar lavage fluid obtained 5 min after antigen challenge [31].
• Procaterol was rapidly absorbed after oral administration [32].
• 2. The vasopressor response induced by electrical stimulation of the preganglionic sympathetic nerve fibres was increased by procaterol, whereas the increase in blood pressure evoked by exogenous noradrenaline was not affected [33].

References