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At least 19 recordsLinked to original sources

PubMed1976

[Profile of pharmacological actions of NAB 365 (clenbuterol), a novel broncholytic agent with selective activity on adrenergic beta2-receptors (author's transl)].

Effects of 4-amino-alpha-[(tert.-butylamino)methyl]-3,5-dichlorobenzyl alcohol hydrochloride (clenbuterol, NAB 365) on the adrenergic beta-receptors were investigated and compared with those of isoproterenol and salbutamol. The beta2-mimetic activity of clenbuterol on the smooth muscle of bronchi, uterus and vessels after i.v. injection corresponds to that of salbutamol in all laboratory animals. When given subcutaneously or as an aerosol clenbuterol is even somewhat more effective than isoproterenol. Clenbuterol differs from the known beta-mimetic drugs in its much longer duration of action. Therefore the integral of activity of single doses of clenbuterol, which are equally effective in the period of their maximal action, is remarkably greater than that of the other beta-mimetic substances. Clenbuterol differs from known beta-mimetic drugs used as bronchodilators in its efficacy after oral administration and in its mode of action on the heart. In the isolated auricle of the rabbit it has proved to be a weak partial agonist. In conscious rabbits, anesthetised guinea-pigs, dogs and cats the maximum of tachycardia obtainable by clenbuterol is lower than that of salbutamol. The higher degree of tachycardia in conscious dogs provoked by clenbuterol is a result of a reflex reaction to the vasodilation analogous to that of salbutamol. In higher doses clenbuterol shows beta1-blocking properties. Like other beta-blocking agents it owns qualities of a local-anesthetic and prolongs refractory period of the heart of guinea-pigs. In contrast to other beta-mimetic substances, clenbuterol causes only slight mobilization of heart muscle glycogen by doses higher than those which have broncholytic effects. The lipolytic and lactacidemia inducing activity of clenbuterol in rabbits corresponds to that of isoproterenol. The blood sugar is only slightly increased by clenbuterol as well as by other beta-mimetic agents. Degree and duration of action of clenbuterol and the other sympathomimetic amines on skeletal muscle of the cat shows parallelism with that of the broncholytic effect. In the rat clenbuterol inhibits the gastric secretion more than does isoproterenol. In contrast to other broncholytic substances, a very small dosage of clenbuterol is sufficient to protect rats against the liberation of histamine and serotonin caused by the anaphylactic reaction.

Adrenergic beta-Agonists↗

PubMed1992

Effects of a beta 2-agonist (clenbuterol) on cultured human (CG-5) breast cancer cells.

In order to gain further knowledge about the possible oestrogen-like activities of clenbuterol (a beta 2-adrenergic drug illegally used as partitioning agent in food producing animals), we treated a hormone dependent human breast cancer cell line (CG-5) with different concentrations of the drug (10(-3) M to 10(-8) M). The effects of clenbuterol and oestradiol on cell proliferation were compared. Both oestradiol and clenbuterol, at low concentrations (10(-7) M and 10(-8) M) stimulated cell proliferation, but the effects of clenbuterol were less marked and significant. Probably clenbuterol elicited cell proliferation through a different mechanism, since it did not affect the cellular oestrogen receptor concentration. Clenbuterol failed in binding to the high affinity oestrogen receptors present in the CG-5 cells. As the beta-adrenergic receptors and the susceptibility to their stimulation have been recently demonstrated in vivo and in vitro in many tumour and normal cells, it is reasonable to suppose that clenbuterol may induce cell proliferation through beta-adrenergic stimulation.

Breast Neoplasms↗

PubMed1992

Effect of the beta-adrenoceptor agonist clenbuterol and phytohaemagglutinin on growth, protein synthesis and polyamine metabolism of tissues of the rat.

1. The kidney bean lectin, phytohaemagglutinin (PHA), induced a marked atrophy of skeletal muscle which was evident from the changes in tissue composition (protein, RNA, DNA and polyamine content) and from the reduction in weight and protein synthesis of hind leg muscles of rats fed on kidney bean-diets for four days. The beta-adrenoceptor agonist, clenbuterol, induced skeletal muscle hypertrophy by transiently stimulating protein synthesis. As a consequence, the muscle loss caused by a short exposure to PHA was, in part, ameliorated by clenbuterol treatment. 2. Cardiac muscle was affected to a lesser extent than skeletal muscle by both clenbuterol and the lectin. However, there was evidence that protein synthesis in heart was reduced by PHA. 3. PHA had opposite effects on the gut, the lectin-induced hyperplasia of the jejunum was accompanied by a large increase in protein synthesis. Clenbuterol alone had no effect on the jejunum whereas a combination of PHA and clenbuterol appeared to exacerbate the effect of the lectin on gut. 4. Both the lectin-induced gut growth and the hypertrophy of skeletal muscle caused by clenbuterol were preceded by the accumulation of polyamines in the respective tissues. Of particular note was the observation that a significant increase in the proportion of the intraperitoneally injected 14C-labelled spermidine or putrescine taken up by the growing tissues could be detected by the second day. Therefore, the measurement of uptake of labelled polyamines may be used as a sensitive indicator of early alterations in tissue metabolism.

Animals↗

PubMed1992

Anabolic effects of clenbuterol on skeletal muscle are mediated by beta 2-adrenoceptor activation.

The potent anabolic effects of the beta 2-adrenoceptor agonist clenbuterol on skeletal muscle have been reported to be independent of actions on beta-adrenoceptors. In the present study clenbuterol, presented to rats in the diet (4 mg/kg), caused significant increases in gastrocnemius muscle mass, protein, and RNA content and a decrease in epididymal fat pad mass. These effects were not mimicked by oral administration of the beta 2-adrenoceptor agonist salbutamol even at high dose (52 mg/kg diet), and the effects of clenbuterol were not inhibited by addition of DL-propranolol (200 mg/kg diet). However, the selective beta 2-antagonist ICI-118,551 (200 mg/kg diet) reversed the anabolic effects of clenbuterol, and a high dose of DL-propranolol (1,000 mg/kg diet) also inhibited these actions of clenbuterol. Furthermore, continuous infusion of salbutamol (1.15 mg.kg body wt-1.day-1) via miniosmotic pumps did cause significant increases in muscle mass, protein, and RNA content. These results indicate that the anabolic effects of clenbuterol are dependent on interaction with the beta 2-adrenoceptor. However, a long duration of action appears to be required to induce the anabolic effects of beta 2-agonists.

Albuterol↗

PubMedDate not supplied

Hemodynamic effects on hepatic blood flow of a selective beta 2-adrenoceptor agonist, clenbuterol, in rat.

Acute clenbuterol administration (50 micrograms/kg, i.v.) to anesthetized normotensive rats, produce a marked reduction in the mean blood pressure, (MBP), about 58 mm Hg. Indocyanine Green clearance analysis (control, 1.83 +/- 0.15: clenbuterol, 1.10 +/- 0.20 ml/min/100 g, P < 0.05) showed that the action in the hepatic vascular bed is opposite to its systemic vasodilator effects. The hepatic blood flow (HBF) appears significantly reduced (control, 8.24 +/- 0.35: clenbuterol, 3.83 +/- 0.71 ml/min/100 g, P < 0.05) whereas the hepatic uptake and excretion proceedings were apparently not affected (control hepatic extraction coefficient, 0.225 +/- 0.024: clenbuterol, 0.300 +/- 0.04, NS). These findings show that a marked reduction in HBF follows systemic vasodilator effects produced by clenbuterol.

Animals↗

PubMed1992

Modulation of lipoprotein lipase activity in the rat by the beta 2-adrenergic agonist clenbuterol.

This study evaluated the effects of beta 2-adrenoceptor stimulation on some determinants of triglyceride metabolism. Male Sprague-Dawley rats were injected twice daily with clenbuterol (30 micrograms.kg-1) for 7 days, or with an equivalent volume of vehicle. Serum triglycerides, hepatic triglyceride secretion rate, and lipoprotein lipase activity in white and brown adipose tissues as well as in red vastus lateralis muscle and heart were evaluated in the fasting state and following a fat-free, high-sucrose meal, 3 h after the last agonist injection. In rats killed in the fasting and postprandial states, clenbuterol reduced the mass of white adipose tissue (-25 and -12%, respectively; p < 0.02), whereas it increased the mass of vastus lateralis muscle (+11 and +7%; p < 0.002) and heart (+13 and %; p < 0.0001). In vehicle-injected animals, the fasting state was associated with lower lipoprotein lipase activity in white and brown adipose tissues, and higher enzyme activity in vastus lateralis and heart, compared with the postprandial state. Postprandially, treatment with clenbuterol reduced lipoprotein lipase activity in white adipose (-24%), whereas it increased enzyme activity in brown adipose (+107%) as well as in vastus lateralis (+35%). In fasted animals, no significant variation of enzyme activity in these tissues was observed following clenbuterol treatment, whereas in the heart, a decrease of lipoprotein lipase activity was observed (-22%). Clenbuterol lowered serum triglycerides significantly (-23%), but not their rate of secretion, whereas the agonist decreased the insulin to glucagon ratio only in the postprandial state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1976

Selectivity of clenbuterol (NAB 365) in guinea-pig isolated tissues containing beta-adrenoceptors.

The effects of clenbuterol (ANB 365), an aminohalogen substituted phenylethanolamine, have been examined on isolated tissue preparations from guinea-pigs. Clenbuterol produced concentration (or dose)-dependent relaxations of tracheal chains, decreases in perfusion pressure of hind limb blood vessels, inhibitions of acetylcholine-induced contractions of the uterus, increases in atrial rate and inhibitions of electrically-induced contractions of the ileum. These responses were blocked by propranolol. Clenbuterol was similar in potency to isoprenaline on the trachea (carbachol-contracted), hind limb and uterus (beta2-adrenoceptors) but was significantly less potent than isoprenaline on the atria and the ileum (beta1-adrenoceptors). Clenbuterol produced marked relaxation of intrinsic tone tracheal preparations in concentrations up to 3000 times less than were required on carbachol-contracted preparations, whereas for isoprenaline the concentrations required on intrinsic tone preparations were only 55 fold less. It is concluded that clenbuterol is a beta-adrenoceptor agonist and that it is a partial agonist on the carbachol-stimulated trachea, on the atria and on hind limb blood vessels. It shows beta2-selectivity in that its potency, relative to that of isoprenaline, on the preparations containing beta2-adrenoceptors was much higher than on those with beta1-adrenoceptors. On intrinsic tone tracheal preparations it may produce an additional relaxant effect responsible for its high potency on that preparation.

Adrenergic beta-Agonists↗

PubMed1979

Dose response relationship of clenbuterol (NAB 365) as a solution for inhalation.

The dose-response relationship of the new bronchodilator Clenbuterol (NAB 365, Boehringer Ingelheim) was tested in 12 patients with chronic obstructive lung disease. Clenbuterol is a beta-2-sympathicomimetic, from a series of substituted phenylethanolamines, and it is characterised by good absorption and prolonged action after systemic administration. The action of four different doses of Clenbuterol inhalation solution (6, 12, 24, and 48 microgram corresponding to 2, 4, 8 and 16 drops of a 0.006% solution) was assessed after a single inhalation on 4 successive days. The parameters monitored were bronchial resistance and FEV. The effect of all four doses was the same, both in respect of improvement in FEV and of decrease in bronchial resistance. The increase in expiratory volume and the decrease in bronchial resistance lasted for 6 h. The results show that for inhalation therapy Clenbuterol is a potent, selective bronchodilator, which is largely free of sideeffects. It has still to be determined whether a maximal effect could be achieved with a lower dose 6 microgram.

Adult↗

PubMed1992

Influence of clenbuterol on the protein digestibility and on nitrogen balance in rats.

1. The influences of a beta-agonist, clenbuterol, on the fecal and urinary nitrogen excretion, the protein digestibility and the nitrogen balance and retention in female Wistar rats of three different weights (70, 150 and 200 g) have been studied. 2. The addition of clenbuterol to the diet did not alter the fecal nitrogen excretion, nor did it change the digestibility coefficient of the protein, irrespective of the age/weight of the animals and the amount of the beta-agonist used. 3. Clenbuterol decreased the urinary nitrogen excretion, especially in older/heavier animals and fed diets with the same dose of the agonist. 4. Nitrogen balance and retention, which, as expected, decrease as the age/weight of the animals decreases, increased significantly with the use of clenbuterol, especially in older/heavier animals. 5. From the results of this study, it can be concluded that, for the range of weight studied, the effect of this beta-agonist does not show on the absorption of proteins at the digestive level; at a metabolic level, however, it does affect the nitrogen retention although, again, to a greater extent in older/heavier animals.

Aging↗

PubMedDate not supplied

The digestive and metabolic utilization of the dietary protein: effect of clenbuterol and protein level.

The influence of a beta-agonist, clenbuterol, added to the diet at 0, 30 and 50 mg/Kg was studied on the digestive and metabolic use of the dietary protein in Wistar rats of two different weights (70 and 200 g). The rats had been fed diets containing different protein levels (4, 10 and 15%). Treatment with clenbuterol did not have any effects on the absorption of the dietary protein in any of the studies released. The beta-agonist did not alter fecal nitrogen excretion nor did it change the digestion coefficient of the protein at the doses used. Clenbuterol significantly increased (P less than 0.01) urinary nitrogen excretion in younger animals fed diets containing low levels of protein (4%). On the other hand, in animals of greater age/weight that had been fed diets with a sufficient protein content (15%), the beta-agonist significantly reduced urinary nitrogen excretion (P less than 0.001). From the results of this study, it can be concluded that in order that clenbuterol can significantly increase nitrogen balance and protein retention, the animals must be given a sufficient exogenous protein intake and they must not be at a stage of maximum growth potential.

Absorption↗

PubMed1992

Satellite cells in innervated and denervated muscles treated with clenbuterol.

The sympathomimetic agent, clenbuterol, induces a muscle-specific hypertrophy in both normal and catabolic muscle. Drug-induced hypertrophy is not generally associated with an increase in DNA content, thus the role of satellite cells in the response of soleus muscles from weanling rats is questioned. Following simultaneous sciatic section and administration of clenbuterol, responses are similar in innervated and denervated muscles after 4 days. Increased protein accretion in treated muscles is associated with evidence of satellite cell activation, but with little evidence of division. It is speculated that satellite cell production of growth factors may play an important role in the hypertrophic action of clenbuterol, and the clinical implications of the findings are discussed.

Animals↗

PubMed1992

Effect of clenbuterol on skeletal muscle atrophy in mice induced by the glucocorticoid dexamethasone.

1. The ability of clenbuterol to antagonize the catabolic effect of the glucocorticoid dexamethasone on the skeletal muscles, soleus, gastrocnemius and extensor digitorum longus was studied in mice. 2. Daily injections of 5 mg dexamethasone/kg body weight over 10 days caused a significant (20%) loss of muscle weight and protein content in fast twitch but not in slow twitch muscles. 3. Inclusion of clenbuterol (4 mg/kg) in the diet for the period of dexamethasone treatment partly prevented glucocorticoid-induced muscle atrophy, and increasing the concentration of clenbuterol to 8 mg/kg diet totally prevented glucocorticoid-induced protein loss in all muscles.

Animals↗

PubMed1992

Stimulation of actin and myosin synthesis in rat gastrocnemius muscle by clenbuterol; evidence for translational control.

1. A transient rise in fractional rates of protein and actomyosin synthesis was observed in gastrocnemius muscles of rats fed clenbuterol for 1-2 days but the muscle RNA:protein ratio was unchanged, therefore protein synthesis per unit RNA (kRNA) also increased. 2. Myosin heavy and light chains and actin showed increased incorporation of [3H]phenylalanine at 2 days; these changes were proportional to increases in total protein synthesis. 3. The ratios actin mRNA:18S RNA and fast myosin heavy chain mRNA:18S RNA were unaffected by clenbuterol. 4. The data suggest that the clenbuterol-induced increase in muscle protein synthesis involves both translational control and increased tissue RNA.

Actins↗

PubMed1992

Respiratory mechanics of horses during stepwise treadmill exercise tests, and the effect of clenbuterol pretreatment on them.

Normal Standardbred horses were given an incremental exercise test on a horizontal treadmill to evaluate the influence of exercise on gas exchange, resistance, dynamic compliance and inertance of the respiratory system. The exercise test consisted of 2 min exercise steps at each of the following speeds: 2.4 m/sec (walk), 4.5 m/sec (slow trot), 7.0 m/sec (fast trot) and 10 m/sec (gallop). At rest and after 1 min of exercise at each step, airflow, tidal volume, respiratory frequency, pharyngeal, mid-oesophageal and transdiaphragmatic pressures and arterial blood gas tensions were measured. The same horses were subsequently treated intravenously with clenbuterol (0.8 microgram/kg) and an identical exercise test and measurement performed 10 min after clenbuterol injection. In response to exercise, there were large increases in tidal volume, respiratory frequency, airflow and pressures. Exercise was associated with a decrease in upper airway resistance but total pulmonary resistance was unchanged. Exercise did not alter inertance or dynamic compliance, horses became hypoxaemic, and at 10 m/sec (galloping) also developed hypercarbia. Treatment with clenbuterol did not alter any of these measurements in response to exercise. These data suggest that dilation of upper airways occurs during exercise, and that inertial forces are important in strenuously exercising horses and may influence the accuracy of dynamic compliance determinations at high exercise intensities.

Airway Resistance↗

PubMed1977

A trial of clenbuterol in bronchial asthma.

Clenbuterol is a beta 2-sympathomimetic bronchodilator. In a double-blind cross-over trial in 19 asthmatic patients with reversible airways obstruction, oral administration of both clenbuterol (40 microgram) and salbutamol (4 mg) caused significantly greater increased in peak expiratory flow rate (PEFR) than placebo, that of clenbuterol lasting longer. The patients' subjective assessment also suggested the relief of their symptoms by the active drugs. Side-effects were minimal.

Adolescent↗

PubMed1979

Aerosolized clenbuterol (NAB 365) and salbutamol in exercise-induced asthma.

The effect of clenbuterol (NAB 365) in inhibiting exercise-induced asthma was compared with that of salbutamol in a single-blind, placebo-controlled, crossover study. Single doses of 20 microgram clenbuterol and 200 microgram salbutamol were given by inhalation 180 minutes before exercise to 9 patients. The exercise used was treadmill running. Clenbuterol offered complete protection to 7 patients, partial protection to 1 and no protection to 1 patient. Salbutamol offered complete protection to 5 patients, partial protection to 1 and no protection to 3 patients. One patient was not protected by any treatment. The protective effects of the two beta-adrenergic bronchodilator drugs were similar (p = 0.42 for FEV1 and p = 0.10 for FEF25-75%). Placebo failed to prevent exercised-induced asthma in any patient. No adverse reactions were manifested or reported by the patients.

Adolescent↗

PubMed1992

The effect of the beta-adrenergic agonist clenbuterol on growth and protein metabolism in rat muscle cell cultures.

Cultures were established from neonatal rat muscle cells, satellite cells, and L6 myoblasts and changes in protein metabolism were determined as development proceeded. For all three cell types, culture protein content increased with increasing myotube content. The beta-adrenergic agonist clenbuterol (added to a final concentration of 10(-7) M) significantly stimulated fusion (as indicated by creatine kinase activity) in neonatal muscle cultures and also increased culture protein content. This was associated with a stimulation in both the fractional (ks, percentage/day, +13%, P less than .05) and absolute (As, micrograms/day, +19%, P less than .05) rates of protein synthesis within 24 h after drug administration. At 48 h, As was increased by 42% above that of controls (P less than .01). In contrast, in satellite cell cultures, clenbuterol had no consistent effects on either protein accretion, creatine kinase activity, or protein synthesis (ks and As). Similarly, the drug had no stimulatory effect on protein synthesis and protein accretion in L6 myoblast or L6 myotube cultures (and no effect in neonatally derived fibroblast cultures). It is concluded that the fusion response to clenbuterol and, therefore, changes in protein metabolism and protein accretion are greatly dependent on the origin and genetic integrity of muscle cells.

Animals↗

PubMed1992

The effects of clenbuterol on satellite cell activation and the regeneration of skeletal muscle: an autoradiographic and morphometric study of whole muscle transplants in mice.

The beta-2 agonist clenbuterol was tested for its effect on the proliferation of satellite cells in transplanted skeletal muscles. Using autoradiographic techniques it was found that satellite cells in clenbuterol treated transplants began proliferating earlier than in control animals. The effect of clenbuterol on the growth of regenerating muscle fibres was also examined using morphometric techniques, which manifested itself as hypertrophy of the fibres when compared with the controls.

Animals↗