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At least 199 records · Page 11Linked to original sources
PubMed2002

Effects of selective beta2 and beta3-adrenoceptor agonists on detrusor hyperreflexia in conscious cerebral infarcted rats.

PURPOSE: We evaluated the effects of beta-adrenoceptor agonists on detrusor hyperreflexia in cerebral infarcted rats. MATERIALS AND METHODS: To produce cerebral infarction in Sprague-Dawley rats the left middle cerebral artery was occluded by introducing a monofilament nylon thread into the artery. In sham operated rats the same artery was exposed but not occluded. After these operations cystometric and cardiovascular experiments were performed with no anesthesia or restraint. RESULTS: After the operation bladder capacity was significantly decreased and voiding pressure was significantly increased in cerebral infarcted but not in sham operated animals. The difference in cerebral infarcted and sham operated rats was significant for each parameter (p <0.01). Post-void residual urine volume was not affected in either group. In the cerebral infarction group intravenous administration of CL316243 ([R,R]-5-2-[[2-(3-chlorophenyl-2-hydroxyethyl]-amino]propyl] -1,3-benzodioxole-2,2-dicarboxylate) (Kissei Central Laboratories, Hotaka, Japan) a selective beta3-adrenoceptor agonist, significantly increased bladder capacity at 10 and 100 microgram./kg. without affecting voiding pressure or post-void residual urine volume. Procaterol, a selective beta2-adrenoceptor agonist, significantly increased bladder capacity and post-void residual urine volume at 10 microgram/kg. intravenously without affecting voiding pressure. In separate experiments procaterol (1 to 100 microgram./kg. intravenously) decreased mean blood pressure and increased heart rate in a dose dependent manner. In contrast, the effects of CL316243 (0.1 to 100 microgram./kg. intravenously) on mean blood pressure and heart rate were minimal. CONCLUSIONS: These results indicate that in cerebral infarcted rats detrusor hyperreflexia can be suppressed by the selective beta3-adrenoceptor agonist CL316243 without increasing post-void residual volume and without significant cardiovascular side effects. If the current results hold true in humans, selective beta3-adrenoceptor agonists may prove useful for treating detrusor hyperreflexia associated with cerebral infarction.

Adrenergic beta-2 Receptor Agonists↗
PubMed2002

Fenoterol inhibits superoxide anion generation by human polymorphonuclear leukocytes via beta-adrenoceptor-dependent and -independent mechanisms.

BACKGROUND: Beta2-adrenoceptor agonists, used widely as bronchodilator in treating bronchial asthma, may have anti-inflammatory activity. OBJECTIVE: We examined whether various widely prescribed beta2-adrenoceptor agonists differ in anti-inflammatory mechanisms. METHODS: We investigated effects of these drugs on superoxide anion generation by stimulated human polymorphonuclear leukocytes in vitro using chemiluminescence. RESULTS: At high concentrations, fenoterol significantly inhibited both N-formylmethionyl-leucyl-phenylalanine- and phorbol myristate acetate-induced superoxide generation by neutrophils. In contrast, salbutamol or procaterol partially inhibited generation with the former stimulus but not the latter. Inhibition by salbutamol or procaterol was completely reversed by either propranolol, a nonselective beta-adrenoceptor antagonist, or ICI-118551, a beta2-adrenoceptor-selective antagonist. In contrast, the effect of fenoterol at concentrations exceeding 10(-6) M against superoxide generation with the former stimulus was only partially reversed by antagonists, and the effect of high concentrations of fenoterol against generation with the latter stimulus was not reversed. No drugs scavenged superoxide at the highest concentration used (10(-5) M). CONCLUSIONS: Fenoterol at high concentrations has an inhibitory effect on superoxide generation that includes a component not mediated via beta2-adrenoceptors. Direct inhibition at or downstream from protein kinase C may be involved.

Adrenergic beta-Agonists↗
PubMed2003

Beta2-adrenergic receptor antagonist accelerates skin barrier recovery and reduces epidermal hyperplasia induced by barrier disruption.

Effects of topical application of adrenergic receptor agonists and antagonists on epidermal barrier repair rate after barrier disruption were studied. Agonists and antagonists of beta1-adrenergic receptor did not affect the barrier repair rate. On the other hand, beta2-adrenergic receptor agonists, procaterol and alprenol, delayed barrier recovery and the beta2 receptor antagonist, ICI-118551, blocked the delay. Moreover, topical application of ICI-118551 or beta1,2 receptor antagonist, clenbuterol alone accelerated barrier recovery. Antagonists of alpha1 and alpha2 receptors did not affect barrier recovery. The delay of barrier repair induced by prodaterol hydrochloride was blocked by a voltage-gated calcium channel blocker, verapamil or nifedipine. In cultured human keratinocytes, procaterol increased the intracellular calcium concentration and the increase was blocked by ICI-118551 and also by verapamil or nifedipine. Topical application of ICI-118551 partially blocked the epidermal hyperplasia induced by acetone treatment under low environmental humidity. These results suggest that the beta2-adrenergic receptor is specifically associated with skin barrier homeostasis.

Adrenergic beta-2 Receptor Antagonists↗
PubMed2005

Beta2-adrenoceptor agonists induce the mammalian clock gene, hPer1, mRNA in cultured human bronchial epithelium cells in vitro.

The mammalian Per1 gene is one of the most important components of circadian clock function of the suprachiasmatic nucleus and peripheral tissues. We examined whether the beta2-adrenoceptor agonists, procaterol and fenoterol, induce human Per1 mRNA expression in human bronchial epithelium. The in vitro stimulation of beta2-adrenoceptor agonists in BEAS-2B cells led to a remarkable increase in the level of hPer1 mRNA. Moreover, fenoterol or procaterol induced the phosphorylation of CREB in BEAS-2B cells as verified by immunoblot analysis. beta2-adrenoceptor agonists induced human Per1 mRNA expression by the signaling pathways of cAMP-CREB in BEAS-2B cells.

Adrenergic beta-2 Receptor Agonists↗
PubMed1984

The classification of beta-adrenoceptors in isolated ring preparations of canine coronary arteries.

Relaxant responses to the beta-adrenoceptor agonists isoprenaline, fenoterol, noradrenaline or procaterol were obtained on isolated ring preparations of canine coronary arteries contracted with KCl (20 mM) or 5-hydroxytryptamine (3 microM). On left circumflex arterial preparations, Schild plots for the selective antagonists atenolol (beta 1-selective) or ICI 118,551 (beta 2-selective), when using noradrenaline or fenoterol as agonist, were superimposed. This suggested that only one subtype of beta-adrenoceptor was involved in the responses. The pA2 values on left circumflex artery preparations were: atenolol, noradrenaline as agonist 6.98, fenoterol as agonist 6.71; ICI 118, 551, noradrenaline as agonist 6.66, fenoterol as agonist 7.04. These data indicated that the beta-adrenoceptor subtype was beta 1. The relative potencies of isoprenaline: noradrenaline: fenoterol were left circumflex 100: 10.0: 2.3, left ventricular branch 100: 9.7: 2.0, septal branch 100: 10.9: 2.5. These data confirmed that beta 1-adrenoceptors were involved in the responses of all three arterial preparations. On preparations of left circumflex artery, left ventricular branch and septal branch, responses were obtained to high concentrations (1 to 100 microM) but not to low concentrations (0.001 to 0.1 microM) of procaterol. This observation confirmed the absence of beta 2-adrenoceptors in these arteries. Responses of left circumflex artery to isoprenaline were potentiated by the extraneuronal uptake inhibitor drugs, corticosterone and metanephrine. 7 It is concluded (a) that responses of canine left circumflex artery, left ventricular branch and septal branch are mediated by a homogeneous population of beta 1-adrenoceptors, and (b) that modulation of responses to isoprenaline by extraneuronal uptake is not confined to responses mediated by beta 2-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1985

Identification of presynaptic beta 2-adrenoceptors on the sympathetic nerve fibres of the human pulmonary artery.

Strips of human pulmonary arteries from patients undergoing surgery for lung tumour were incubated with [3H]-noradrenaline. Subsequently, they were superfused with physiological salt solution containing cocaine and corticosterone. Tritium overflow from the strips was stimulated by transmural electrical impulses (2 Hz). The electrically evoked overflow of tritium consisted of 91% unmetabolized [3H]-noradrenaline, and this percentage was not altered by isoprenaline. 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 considerably less active than the previously mentioned agonists; noradrenaline (in the presence of rauwolscine) was ineffective. The concentration-response curve of procaterol was shifted to the right by the preferential beta 2-adrenoceptor antagonist ICI 118-551 but was not affected by the beta 1-selective antagonist, atenolol. Propranolol, but not atenolol, produced a shift to the right of the concentration-response curve of isoprenaline. It is concluded that the sympathetic nerve fibres of the human pulmonary artery are endowed with facilitatory presynaptic beta 2-adrenoceptors.

Cocaine↗
PubMed1992

The role of cyclic AMP in non-adrenergic non-cholinergic contraction in guinea-pig bronchi.

1. We investigated the role of adenosine 3':5'-cyclic monophosphate (cyclic AMP) in non-adrenergic non-cholinergic (NANC) contraction in guinea-pig bronchial strips. 2. Forskolin (3 nM to 1 microM) reduced NANC contraction induced by electrical field stimulation (EFS) in a concentration-dependent fashion (-log EC50 was 7.22 +/- 0.12 M and maximum inhibition was 100 +/- 0.01%). However, forskolin (less than 1 microM) did not alter the contraction induced by substance P (SP, 1 microM). 3. Dibutyryl cyclic AMP (1 mM) also reduced NANC contractions induced by EFS (100 +/- 0.01%) without significant effect on SP (1 microM)-induced contractions. In contrast, dibutyryl cyclic GMP (1 mM) was without effect against either NANC or SP-induced contractions. 4. Both the beta 2-adrenoceptor agonist, procaterol (0.1 nM to 3 nM) and theophylline (100 nM to 1 mM) concentration-dependently reduced EFS-induced NANC contractions without significant effect on SP (1 microM)-induced contractions. 5. In contrast to forskolin, procaterol and theophylline, both sodium nitroprusside and cromakalim inhibited the EFS-induced contractions only at those concentrations that similarly reduced the contractions induced by SP (1 microM). 6. These results suggest that cyclic AMP may mediate pre-junctional inhibition of NANC contractions in guinea-pig bronchi.

Animals↗
PubMed1986

Further studies on the cardiomegaly induced by beta-adrenoceptor agonists.

Rats received continuous infusions of beta-adrenoceptor agonists by means of Alzet osmotic minipumps implanted subcutaneously. After 7 days of isoprenaline infusion (2 mg/kg per day) the heart/body weight ratio increased about 40 per cent compared with placebo treatment. The difference persisted after freeze-drying indicating a true hypertrophy and not merely an oedema. When terbutaline (20 mg/kg per day) was substituted for isoprenaline, the increase in wet weight ratio reached only about 5 per cent. Procaterol (2 mg/kg per day) and pirbuterol (20 mg/kg per day) had no effect on the heart weight. It is concluded that in doses expected to cause comparable stimulation of beta 2-adrenoceptors the unselective agonist isoprenaline is able, more than the beta 2-selective agonists terbutaline, procaterol and pirbuterol to cause cardiac hypertrophy thus indicating the involvement of beta 1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1992

Beta 2-adrenoceptor-mediated positive dromotropic effects on atrioventricular node of dogs.

The functional significance of beta 2-adrenoceptors in atrioventricular (AV) nodal conduction was investigated by using canine isolated blood-perfused AV node preparations. Dose-dependent shortening of the atrio-His bundle (A-H) interval by dl-procaterol hydrochloride hemihydrate (0.03-1 nmol) injected intra-arterially into the AV node artery was affected little by an infusion of dl-atenolol (10 nmol/min) into the same artery, whereas the dose-response curve for the positive dromotropic effect of procaterol was shifted markedly to the right by approximately 1.5 and 2.5 log units with ICI 118551 [erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylamino-bu tan-2-ol]- hydrochloride (1 and 10 nmol/min). The positive dromotropic effect of dl-T-1583 [alpha-(3,4,5-trimethoxyphenethylaminomethyl)-3,4-dihydroxybenzyl- alcohol] hydrochloride (30-300 pmol), a selective beta 1-adrenoceptor agonist, was shifted to the right by approximately 1.2 log units with dl-atenolol (10 nmol/min) but was affected little by ICI 118551 (10 nmol/min). The dose-response curve for l-isoproterenol hydrochloride (3-100 pmol) was shifted to the right by 0.7 log unit with ICI 118551 (10 nmol/min) and by 1.7 log units with atenolol (10 nmol/min). The dose-response curve for dl-norepinephrine (0.03-1 nmol) was shifted to the right by 1.0 log unit with atenolol only, whereas the curve for l-epinephrine (0.03-1 nmol) was shifted by 0.45 log unit with ICI 118551 (10 nmol/min). These results suggest that both beta 1- and beta 2-adrenoceptors, which coexist on the AV node, play a functional role in AV nodal conduction.

Adrenergic beta-Agonists↗
PubMed2004

Heterogeneous beta2-adrenoceptor expression and dilation in coronary arterioles across the left ventricular wall.

BACKGROUND: Previous in vivo studies have shown that beta-adrenoceptor agonists cause a redistribution of coronary flow away from the subendocardium; however, the underlying mechanism remains uncertain. We tested the hypothesis that a heterogeneous distribution of beta-adrenoceptors and their vasomotor responses exists in the coronary microcirculation across the left ventricular wall. METHODS AND RESULTS: Porcine subepicardial and subendocardial arterioles (<100 microm) were isolated from the left ventricle and pressurized for in vitro study of vasodilation to the nonselective beta-adrenoceptor agonist isoproterenol and the selective beta2-adrenoceptor agonist procaterol. Both vessel types developed a similar level of basal tone and dilated to isoproterenol and procaterol. However, subepicardial arterioles exhibited a much higher sensitivity and greater dilation capacity to both agonists. The isoproterenol-induced vasodilations were inhibited by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker. In contrast to isoproterenol, dilations of subepicardial and subendocardial arterioles to pinacidil, a K(ATP) channel opener, were similar. In both vessel types, isoproterenol-induced dilation was inhibited by the beta2-adrenoceptor blocker ICI-118,551 but was insensitive to the beta1-adrenoceptor blocker atenolol. Reverse transcription-polymerase chain reaction and immunohistochemical data revealed that beta2-adrenoceptor mRNA and protein expression, respectively, were markedly greater in subepicardial arterioles. CONCLUSIONS: This study demonstrates that selective activation of beta2-adrenoceptors elicits dilation of both subepicardial and subendocardial arterioles through opening of K(ATP) channels. The higher beta2-adrenoceptor expression in subepicardial arterioles may contribute to the greater dilation of these vessels to beta2-adrenoceptor activation.

Adrenergic beta-2 Receptor Agonists↗
PubMed2001

Clinical characteristics of asthmatic patients prescribed various beta-agonist metered-dose inhalers at Yamagata University Hospital.

To determine the prescription characteristics of beta-agonist metered-dose inhalers (MDI), we retrospectively investigated all prescriptions containing one of five types of beta-agonist MDIs available at Yamagata University Hospital in 1997, as well as patients' characteristics. The total number of asthmatic patients was 225 (age, 11-79, mean, 47.2) in 1997. Fenoterol MDI was prescribed to patients who visited the hospital at regular periods and had more severe asthma. Isoprenaline MDI also was not prescribed for first-time patients. Patients who were prescribed tulobuterol MDI had mild or moderate asthma and some of them were only occasional or first-time visitors. Salbutamol and procaterol MDIs were also prescribed for first-time patients; however, tulobuterol MDI was the most frequently prescribed for first-time patients. Patients prescribed fenoterol and isoprenaline MDIs had adequate knowledge of proper asthma management, because sufficient information had been provided about the use of MDIs in the past. Patients prescribed tulobuterol MDI should be provided with detailed instructions because they had little knowledge of handling MDIs and self-management of asthma as many of them were first or intermittent visitors. Patients prescribed salbutamol or procaterol MDIs should be evaluated regarding their past medications and some of them should be instructed regarding the use of the MDI. Although these clinical aspects might be applicable only to our hospital, the same or other prescription patterns will be found in other hospitals and/or by other physicians. Adequate instructions to individual patients who are prescribed a particular beta-agonist MDI should be provided by the medical staff, especially to outpatients, to reduce hospitalization and death from asthma.

Administration, Inhalation↗
PubMed1992

Bronchodilator-resistive cough in atopic patients: bronchial reversibility and hyperresponsiveness.

The number of atopic patients presenting only chronic non-productive cough appears to be increasing. This study was conducted to confirm the existence of non-asthmatic cough associated with atopy. We prospectively examined atopic findings, therapeutic effects of inhaled procaterol, azelastin, and/or glucocorticoids, improvement of FEV1 by bronchodilator therapy and bronchial responsiveness to methacholine in 20 patients. The cough was relieved by inhaled procaterol in 10 patients (Group 2) but not in the other 10 patients (Group 1). The increase in FEV1 by inhaled salbutamol following aminophylline injection was significantly less in Group 1 than in Group 2. Bronchial responsiveness to methacholine was normal in Group 1 while that in Group 2 was hyperreactive. These findings indicate that there is atopic non-asthmatic bronchodilator-resistive cough (Group 1) which is a different entity from bronchodilator-responsive cough (Group 2), or the so-called "cough variant asthma".

Adrenergic beta-Agonists↗
PubMed1992

Vascular alpha-1 antagonistic and agonistic effects of beta adrenoceptor agonists in rabbit common carotid arteries.

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. In phenylephrine-preconstricted preparations, the three beta agonists induced a dose-dependent vasodilation which was not suppressed by treatment with beta antagonists, atenolol, a selective beta-1 antagonist and ICI 118551, a selective beta-2 antagonist. On the other hand, in prostaglandin F2 alpha-preconstricted preparations, these agonists produced no vasodilation and revealed weak vasoconstrictions which were readily suppressed by bunazosin, a selective alpha-1 antagonist. Moreover, these agonists caused a shift of the dose-response curve for phenylephrine to the right in a parallel fashion in non-preconstricted preparations. The relative pA2 values for isoproterenol, procaterol and denopamine calculated from the displacement curve were 7.47, 7.59 and 8.17, respectively. Thus, it is concluded that 1) there are little functional beta adrenoceptors in the rabbit common carotid arteries, 2) beta adrenoceptor agonists have both antagonistic and agonistic properties for alpha-1 adrenoceptor activation, 3) denopamine possesses a higher potency as an alpha-1 antagonist and 4) beta agonists generally act as vasodilators in rabbit cerebral circulation.

Adrenergic beta-Agonists↗
PubMed1992

[Peripheral airway obstruction and treatment].

The effect of medication on peripheral airway obstruction was examined in cases of bronchial asthma. Subjects were 1) patients with exercise-induced asthma, 2) an animal model of hyperventilation-induced asthma and 3) patients with chronic asthma. Peripheral airway obstruction was induced in 30 of 51 patients with exercise-induced asthma. Induction of peripheral airway obstruction was protected significantly by procaterol. Cromoglycate was effective in 12 of 17 patients but ipratropium was not effective against induction of peripheral airway obstruction. In the animal model, humid air inhalation, procaterol and ipratropium completely prevented hyperventilation-induced bronchoconstriction, but cromoglycate caused only partial prevention. In cases of chronic asthma with peripheral airway obstruction, beclomethasone inhalation reduced the symptom rating rapidly, but no changes were observed in pulmonary function and threshold of airway responsiveness. Cromoglycate was started in patients with chronic asthma who had been treated with beclomethasone. After cromoglycate administration, therapeutic rating decreased, but increased again after 8 weeks of cromoglycate therapy. Peripheral airway obstruction induced by exercise or hyperventilation could be prevented by adequate premedication, but chronic peripheral airway obstruction was difficult to treat.

Administration, Inhalation↗
PubMed1985

Thyroid status and adrenergic receptor subtypes in the rat: comparison of receptor density and responsiveness.

The density and functional responsiveness of adrenergic receptor subtypes were determined in tissues from control, hyperthyroid and hypothyroid rats. There was a decrease in sensitivity to isoproterenol in spontaneously beating right atria, electrically driven left atria and field-stimulated vas deferens associated with hypothyroidism, with no change in maximum response. Hyperthyroidism increased the potency of isoproterenol in right atria, but not in left atria or vas deferens. The maximal response to isoproterenol was greatly reduced in hyperthyroid left atria. The potency of procaterol, a partial agonist at beta adrenergic receptors in right atria, was unaltered in hyper- or hypothyroidism, although the maximum stimulation by procaterol was increased in hyperthyroidism. Scatchard analysis of specific [125I]pindolol binding showed that beta adrenergic receptor density was greater in hyperthyroidism than in hypothyroidism in left atria, right atria, ventricles, vas deferens and cerebral cortex, although the proportions of beta-1 and beta-2 adrenergic receptor subtypes did not change. There was no change in the responsiveness of alpha-1 adrenergic receptors mediating contraction of caudal artery and vas deferens or mediating [3H]inositol phosphate accumulation in cerebral cortex in hyperthyroid or hypothyroid rats, although the maximal contraction of caudal artery was significantly reduced in hyperthyroidism. Scatchard analysis of specific [125I]BE 2254 binding showed that alpha-1 adrenergic receptor density was significantly decreased in the ventricles from hyperthyroid rats and increased in the ventricles of hypothyroid rats, but was unchanged in vas deferens, caudal artery and cerebral cortex. Alpha-2 adrenergic receptor density in cerebral cortex, determined by Scatchard analysis of specific [3H] rauwolscine binding, was not altered in hyperthyroid or hypothyroid rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Characterization of beta-1 and beta-2 adrenoceptors in guinea pig atrium: functional and receptor binding studies.

The selective beta-2 adrenoceptor agonist procaterol produced positive inotropic and chronotropic responses over a concentration range of 1 nM to 0.1 mM in spontaneously beating right atria and in three of seven electrically driven left atria. The pD2 values (right atria, 7.30; left atria, 7.18) were midway between its known affinities at beta-1 and beta-2 adrenoceptors and are evidence that positive inotropic and chronotropic responses involve a minor beta-2 adrenoceptor component. The pKB values for procaterol against (-)-isoproterenol in the right atria (5.59) and left atria (5.29) were consistent with its affinity for beta-1 adrenoceptors and suggest that these are responsible primarily for positive inotropic and chronotropic responses. Receptor binding studies in right atrial homogenates showed that [125I]cyanopindolol binding was saturable (KD = 36.2 pM, maximal density of binding sites = 49.2 fmol mg-1 protein) and stereoselective with respect to the isomers of propranolol. Competition binding curves for the beta-1 adrenoceptor antagonist CGP 20712A and beta-2 selective antagonist ICI 118,551 against [125I]cyanopindolol binding were resolved into two components using iterative curve fitting techniques. Binding sites with the characteristics of beta-1 and beta-2 adrenoceptors were present in the proportions of approximately 75 to 25%. These studies indicate either that the beta-1 adrenoceptor is coupled more efficiently to the positive inotropic and chronotropic response than the beta-2 adrenoceptor or that a proportion of the beta-2 adrenoceptors subserve other functions.

Animals↗
PubMed1984

Adrenaline and the development of genetic hypertension.

The effects, on the development of a raised blood pressure in spontaneously hypertensive (SHR) rats, of bilateral adrenal demedullation and subcutaneous slow-release implants containing adrenaline, salbutamol and procaterol were studied. Systolic blood pressure (SBP) measurements were made, using an indirect tail-cuff method in groups of male SHR rats aged from three to 14 weeks, which were sham-operated or bilaterally adrenal demedullated under ether anaesthesia at four weeks of age. Bilateral adrenal demedullation attenuated the development of a raised blood pressure, while slow-release implants of adrenaline restored the development of hypertension in adrenal demedullated rats and this effect was abolished by concomitant treatment with the beta 2-adrenoceptor antagonist [C] 118551. Implants of salbutamol and procaterol were also effective in restoring hypertension development in adrenal demedullated rats. It is suggested that adrenaline exerts its pro-hypertensive effects via an action at beta 2-adrenoceptors; possibly those located prejunctionally which are involved in the facilitation of sympathetic neurotransmission.

Adrenal Medulla↗
PubMed1993

[Comparison of the bronchodilating effects of five beta-adrenergic stimulants administered by inhalation to patients with bronchial asthma].

The bronchodilating effects of 5 different beta-adrenergic stimulants, isoproterenol, salbutamol, trimetoquinol, orciprenaline and procaterol were examined in 28 same patients who were in a free period from asthmatic attack. Suitable broncho-constrictive conditions for the comparison of the bronchodilators were produced by having the patients inhale methacholine at the threshold dosage, which had been determined previously for each patient. FEV1 measurements were taken throughout the study. Salbutamol was found to be superior to isoproterenol, trimetoquinol and orciprenaline with respect to bronchodilation and its duration. Procaterol, however, showed a more prolonged effect than salbutamol, although the initial bronchodilation was less remarkable.

Administration, Inhalation↗