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PubMed1987

Psychotropic effects of adrenergic beta-blockers on agonistic behavior between resident and intruder mice.

The present study was conducted to investigate the effect of adrenergic beta-blockers on agonistic behavior in male mice, using quantitative ethological methods. Agonistic behavior was evoked using a resident-intruder paradigm. The following drugs were administered orally at four dose levels (vehicle, 5, 10 and 20 mg/kg) to either resident or intruder mice: dl-propranolol, practolol, d-propranolol, and l-propranolol. When the resident was treated with either dl-propranolol or l-propranolol, aggressive episodes (offensive sideways posture, attack bite, tail rattle) were suppressed significantly in a dose-dependent manner, whereas practolol and d-propranolol were ineffective. All treatments except the high dose of l-propranolol failed to affect the resident's solitary behavior (locomotion). When the intruder was treated with beta-blockers, agonistic behavior was not altered. Since practolol does not cross the blood-brain barrier, the differential suppression of agonistic behavior is due to the central action of beta-blockers. d-Propranolol does cross the blood-brain barrier but is devoid of beta-receptor blocking property; hence l-propranolol suppression of agonistic behavior implies inactivation of brain adrenergic beta-receptors. The findings seem to indicate that beta-blockers such as dl-propranolol and l-propranolol have a psychotropic action.

Adrenergic beta-Antagonists↗
PubMed1993

Initial experience with beta blockers in dilated cardiomyopathy.

In early 1973, Waagstein administered bolus intravenous injections of practolol and, subsequently, alprenolol, 50 mg twice daily, to reduce the heart rate of a 59-year-old woman with refractory, idiopathic dilated congestive cardiomyopathy (DCCM) and resting tachycardia. The patient's condition improved dramatically and continued to improve during subsequent oral therapy. This experience, combined with increasing interest in the role of beta blockade in myocardial protection, led to investigation of oral practolol, 50-400 mg twice daily, for 2-12 months in 6 additional patients with advanced DCCM. These findings, published in 1975, indicated improved ventricular function for all participants. In a 1980 open-label follow-up study, 28 patients with DCCM received alprenolol, metoprolol, practolol, or propranolol. Treatment was associated with improvements in myocardial function as well as in related symptomatology. These effects were reversed following drug withdrawal. The findings suggested that beta blockers possessed potential value in treatment of idiopathic DCCM.

Adolescent↗
PubMed1978

Dual effect of adrenalin on sugar transport in rat diaphragm muscle.

The effect of adrenalin on the membrane transport of the non-metabolized sugar, 3-methylglucose, was studied in isolated "intact" rat hemidiaphragms and related to simultaneously occurring changes in the internal levels of Na+, ATP, glucose-6-P, glycerol formation and 45Ca uptake and loss. Basal sugar transport was inhibited by low (10-8-10-5 M) concentrations of adrenalin; this was antagonized by propranolol and practolol. High concentrations (10-4-10-3 M) stimulated sugar transport, and this was blocked by propranolol and butoxamine and was dependent on external Ca2+. These results suggest interaction with two different classes of adrenergic receptors, possibly of beta 1 and beta 2 types. Both low and high concentrations increases Na+ and K+ gradients by a practolol-sensitive effect. Isoproterenol behaved identically but phenylephrine had only the two practolol-sensitive effects on sugar and ion transport. Insulin did not interfere with inhibition of sugar transport and decrease in internal Na+ but prevented stimulation of sugar transport. Under anoxia adrenalin had no effect on sugar transport but led to greater Na+ gain by tissue. Addition of 3.0 mM palmitate decreased inhibition of sugar transport without changing receptor specificity. ATP was decreased and lipolysis enchanged by high adrenalin but glucose-6-P was increased by the low concentration as well. Influx of 45 Ca was decreased by low and increased by high adrenalin; 45Ca efflux was also differentially affected. The results indicate that inhibition and stimulation of sugar transport depend on different receptors and that the latter response may override the former. The data are consistent with the earlier postulated regulatory role of sarcoplasmic Ca2+ on sugar transport in muscle, with adrenalin affecting Ca2+ fluxes and distribution both directly and indirectly.

Animals↗
PubMed1998

Optimization of mobile phase in the separation of beta-blockers by HPLC.

Beta-blockers are generally determined using high-performance liquid chromatography (HPLC). Previous HPLC separations of beta-blockers have often required a mobile phase containing three components; acetonitrile or methanol to control the retention; buffer to control the ionic strength and pH of the mobile phase; ion-pairing reagent to provide adequate retention of beta-blockers or organic amines as masking agent to reduce peak tailing. Due to the complexity of the mobile phases employed, development of these assays can be a laborious process. Additionally, alkyl sulphonates and organic amines dramatically reduces the life-time reduction of silica based C18 columns. The results of this study demonstrated that the addition of tested alkyl sulphonates and organic amines is not essential for an adequate separation of beta-blockers. In this study, we developed a simple HPLC method for the simultaneous separation of model beta-blockers, atenolol, practolol, metoprolol, oxprenolol and propranolol. Atenolol, practolol, metoprolol, oxprenolol and propranolol adequately separated with high peak symmetries using a mobile phase consisted of methanol/acetonitrile/phosphate buffer (10 mM, pH 3.0) (15:15:70, v/v/v). By altering only the fraction of methanol with respect to acetonitrile, method development becomes a more efficient separation. Furthermore, atenolol, practolol, metoprolol, oxprenolol and propranolol can be detected up to 0.25, 5, 10, 50 and 10 ng ml(-1). In this publication, we present the simultaneous separation of beta-blockers having a wide range of polarity. It is proposed that this new mobile phase, consisting only acetonitrile, methanol and phosphate buffer can be used for the analysis of the several beta-blockers presently in doping control analysis as well as others.

Acetonitriles↗
PubMed1978

Studies of cardioselectivity and partial agonist activity in beta-adrenoceptor blockade comparing effects on heart rate and peak expiratory flow rate during exercise.

1 The effects of beta-adrenoceptor antagonists given in single doses by oral or intravenous routes were examined in two double-blind controlled studies performed in healthy volunteers. Heart rate and peak expiratory flow rate (PEFR) were measured at rest and during standardized exercise. 2 Propranolol 80 mg and metoprolol 100 mg orally tended to reduce, and propranolol and metoprolol 0.2 mg/kg intravenously did reduce the physiological increase in PEFR during exercise; oxprenolol 80 mg orally and 0.2 mg/kg intravenously did not. Practolol 200 mg orally reduced this increase, but practolol 1 mg/kg intravenously did not. 3 In a third study of similar design, pindolol 0.05 mg/kg intravenously did not affect exercise-induced increase in PEFR. 4 Heart rate during exercise was reduced to a comparable extent at different times by all the active treatments. 5 Oxprenolol and pindolol share with practolol the property of partial agonist activity, which might contribute to their apparent lack of effect on airways resistance. A further possibility is that alpha-adrenoceptor blockade helps to maintain exercise-induced increase in PEFR.

Adrenergic beta-Antagonists↗
PubMed1982

Intrinsic sympathomimetic activity and coronary blood flow.

1 The effects of four beta-adrenoceptor blocking agents, propranolol, pindolol, practolol and atenolol, used in doses inducing the same degree of beta 1-adrenoceptor blockade, have been investigated on regional myocardial blood flow (microspheres) and coronary vascular resistance in the normal and ischaemic myocardium of the anaesthetized dog. 2 In the ischaemic and non-ischaemic myocardial areas, transmural blood flow was significantly reduced by propranolol and atenolol which are devoid of intrinsic sympathomimetic activity (ISA) while it remained unaffected by beta-adrenoceptor blocking drugs endowed with ISA, whether cardioselective (practolol) or not (pindolol). In non-ischaemic areas, only propranolol and atenolol increased coronary vascular resistance. 3 Regarding coronary blood flow distribution between the epicardium and endocardium, only propranolol and pindolol induced a favourable redistribution towards the endocardium increasing the endo/epi flow ratio, while practolol and atenolol were ineffective. 4 These results suggest that ISA is of major importance in maintaining coronary flow especially in the ischaemic myocardium but that it is not involved in the mechanisms underlying coronary blood flow redistribution between the different myocardial layers.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

A study of the relationship between cardiac beta-adrenoceptor blockade and intrinsic sympathomimetic activity in rats depleted of catecholamines.

1. The intrinsic sympathomimetic activity of a range of beta-adrenoceptor antagonists and its relationship to beta-adrenoceptor blockade was studied in pentobarbitone-anaesthetized, vagotomized rats which had been depleted of catecholamines by pretreatment with syrosingopine. Dichlorisoprenaline, practolol, oxprenolol, pindolol and acebutolol, produced dose-dependent positive chronotropic responses in this preparation. 2. The relationship between the dose requirements for this intrinsic sympathomimetic activity and beta-adrenoceptor-blocking activity was not the same for all drugs: (i) dichlorisoprenaline and practolol had intrinsic activity at all beta-adrenoceptor-blocking doses; and (ii) oxprenolol, pindolol and acebutolol had predominantly beta-adrenoceptor blockade at the lower dose levels and agonist activity only became significant at high doses relative to those producing beta-adrenoceptor blockade. 3. The positive chronotropic response to both practolol and pindolol was observed in rats which had been pithed and was antagonized by propranolol (0.1-3.0 mg/kg, i.v.), indicating that beta-adrenoceptors were involved. 4. It was concluded that the intrinsic sympathomimetic activity of beta-adrenoceptor antagonists was not a simple property as it was described by the relationship between the dose requirements for intrinsic sympathomimetic activity and for beta-adrenoceptor blockade as well as the degree of partial agonist activity.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The influence of the intrinsic sympathomimetic activity of beta-adrenoceptor antagonists on haemodynamic effects in anaesthetized dogs.

1. The effects of propranolol, atenolol (ICI 66,082), practolol and pindolol on heart rate and maximal left ventricular dp/dt, atrioventricular conduction time, mean aortic flow and diastolic blood pressure during cardiac pacing were investigated over a wide dose range (0.025-4.0 mg/kg, i.v.) in dogs anaesthetized with pentobarbitone.2. Propranolol and atenolol produced similar reductions in haemodynamic parameters. Propranolol had no further effect in dogs pretreated with atenolol. 3. Practolol tended to cause smaller reductions in the haemodynamic parameters than either propranolol or atenolol. Subsequent administration of propranolol still had some depressant activity. 4. Pindolol produced a biphasic response, with depression of cardiac function at the low doses (0.025 and 0.1 mg/kg), but a reversal of effect as the dose was increased. 5. It is therefore concluded that, in anaesthetized dogs, the intrinsic activity of practolol and pindolol limits the fall in heart rate, cardiac conduction, aortic flow and maximal dp/dt observed with beta-adrenoceptor blockade. With pindolol, however, the influence of intrinsic activity is observed only in high doses related to beta-adrenoceptor blockade.

Adrenergic beta-Antagonists↗
PubMed1970

The effect of "selective" beta-adrenoceptor blocking drugs on the myocardial circulation.

1. A comparison has been made of the effects of a relatively specific beta(1)-adrenoceptor blocking drug (practolol) and a relatively specific beta(2)-adrenoceptor blocking drug (butoxamine) on myocardial and general haemodynamics in anaesthetized cats.2. Practolol, in a dose (10 mg/kg, intravenously) which had little effect on arterial pressure, heart rate, myocardial blood flow or myocardial vascular resistance, markedly reduced the effects of isoprenaline infusions on heart rate, aortic dp/dt, myocardial blood flow, vascular resistance and metabolic heat production, and the cardiac effort index. Isoprenaline induced vasodepression was unaffected.3. Butoxamine (5 mg/kg, intravenously) decreased heart rate, aortic dp/dt, the cardiac effort index and myocardial blood flow and increased myocardial vascular resistance. This is taken as further evidence for the existence of beta(2)-adrenoceptors in the myocardial microcirculation.4. After butoxamine, the effects of isoprenaline on myocardial blood flow, myocardial vascular resistance and heart rate were unaffected but the peripheral vasodilator effect was abolished. The effects on aortic dp/dt and the cardiac effort index were potentiated.5. It is concluded that the effect of isoprenaline in increasing myocardial blood flow is due predominantly to increased cardiac work and oxygen consumption and that practolol, since it has little direct effect on myocardial blood flow yet abolishes the cardiac stimulant and oxygen wasting effects of released catecholamines, has properties which indicate that it should be an effective and safe anti-anginal drug.

Acetanilides↗
PubMed1972

Comparative partial agonist activity of -adrenoceptor antagonists.

Inotropic dose-response curves were constructed for a series of beta-adrenoceptor antagonists, based on the inotropic responses of isolated dog trabecular muscles stimulated to contract at a regular rate. Propranolol exerted only a negative inotropic effect but K01366, LB46, oxprenolol and practolol all evoked a positive inotropic response, whether or not catecholamine-depleted muscles were used. The order of potency for this positive inotropic activity was K01366>LB46>oxprenolol>practolol. The duration of the positive inotropic response to the antagonists was more prolonged than that due to isoprenaline. Propranolol significantly reduced the positive inotropic response to K01366, LB46, oxprenolol and practolol.

Acetanilides↗
PubMed1972

The effect of certain -adrenoceptor antagonists on overdrive suppression.

1. Propranolol, as the racemate and the (+)- and (-)-isomers (400 mug/l.) and practolol (50 mg/l.) were tested for their effects on atrial and ventricular rates and on the duration of overdrive suppression (ODI) in isolated perfused cat hearts with surgically-induced heart block.2. Racemic propranolol and the (+)- and (-)-isomers prolonged ODI and slowed the rate of the ventricular pacemaker; the (+)- and (-)-isomers also reduced the rate of the atrial pacemaker. Practolol shortened ODI and increased the rate of the atrial and ventricular pacemakers.3. The (+)- and (-)-isomers were more potent than the racemate; the (-)-isomer was more potent than the (+)-isomer. The results suggest there is a stereospecific mechanism involved in the biological distribution of propranolol.4. Twenty-four hours after reserpine treatment (5 mg/kg, i.p.) practolol continued to increase the rate of the atrial and ventricular pacemakers but did not shorten ODI.5. The mechanism by which these agents affect myocardial excitability and automaticity is discussed.

Acetanilides↗
PubMed1975

The selectivity of beta-adrenoceptor antagonists on cardiovascular and bronchodilator responses to isoprenaline in the anaesthetized dog.

1 The actions of five beta-adrenoceptor antagonists, chosen because of reported differences in their selectivities, were compared using the positive chronotropic, vasodepressor and bronchodilator responses to isoprenaline in anesthetized dogs. 2 Propranolol was a potent antagonist of the isoprenaline responses in all three systems. 3 Practolol and acebutolol (M & B 17,803) blocked the positive chronotropic responses to isoprenaline to a greater extent than the vasodepressor or bronchodilator responses. 4 Butoxamine and alpha-methyl dichloroisoprenaline showed the opposite selectivity, blocking the vasodepressor and bronchodilator responses to isoprenaline to a greater extent than positive chronotropic responses. However, both drugs were considerably less potent than the other antagonists studied and their selectivities were less clear-cut than those of practolol or acebutolol. 5 All the antagonists lowered the resting heart rate and to a lesser extent the diastolic blood pressure. The effects of propranolol, practolol and acebutolol on heart rate probably result from cardiac beta-adrenoceptor blockade. With butoxamine and alpha-methyl dichloro isoprenaline, however, the effects on heart rate probably result from a direct cardiodepressant action. 6 The relevance of the results to the problem of the sub-classification of beta-adrenoceptors is discussed.

Adrenergic beta-Antagonists↗
PubMed1978

The role of beta1- and beta2-adrenoceptors in the inhibition of gastric acid secretion in the dog.

1. Characterization of the beta-adrenoceptors mediating inhibition of gastric acid secretion in the conscious Heidenhain pouch dog has been investigated by determination of the effects of propranolol, (+)-propranolol, practolol and H35/25 on salbutamol and isoprenaline-induced inhibition of gastric acid secretion. 2. The gastric antisecretory effect of salbutamol was significantly blocked by propranolol and H35/25 but not by practolol or (+)-propranolol. The effect of isoprenaline was significantly blocked by propranolol and practolol but not by H35/25 or (+)-propranolol. 3. It is concluded that both beta1- and beta2-adrenoceptors can mediate inhibition of pentagastrin-induced gastric secretion in conscious dogs with a Heidenhain pouch. Salbutamol exerts its antisecretory effect through beta2-adrenoceptors, whereas isoprenaline mediates its effects primarily through beta1-adrenoceptors. 4. The results are discussed with regard to the sub-classification of beta-adrenoceptors and to the possible role of adrenoceptors in the physiological control of gastric secretion. 5. In this study it is concluded that the tachycardia induced by isoprenaline or salbutamol is mediated primarily through reflexes activated by beta2-adrenoceptor mediated vasodilatation.

Albuterol↗
PubMed1984

Is there any evidence of beta 1-adrenoceptors mediating relaxation of guinea-pig lung parenchyma?

We tried to find functional evidence for the existence of beta 1- and beta 2-adrenoceptors in the isolated guinea-pig lung parenchymal strip preparation, using potent and selective beta 1- and beta 2-adrenoceptor stimulation. To obtain potent beta 1-adrenoceptor stimulation the nonselective beta-adrenoceptor agonist isoprenaline was combined with a highly selective beta 2-adrenoceptor antagonist--ICI 118,551. Potent beta 2-adrenoceptor stimulation was obtained by procaterol. Practolol (beta 1-adrenoceptor antagonist) and ICI 118,551 were used as antagonists. ICI 118,551, 10(-7) mol/l, shifted the concentration response (C/R) curve of isoprenaline to a higher concentration range. The C/R curve of procaterol was shifted in the same way and to the same degree by this concentration of ICI 118,551. The C/R curve of isoprenaline was not further shifted after blockade with a combination of ICI 118,551, 10(-7) mol/l, and practolol, 10(-6). However, in the trachea preparation, a tissue containing both beta 1- and beta 2-adrenoceptors, there was a further shift of the C/R curve of isoprenaline to a higher concentration range after blockade with a combination of ICI 118,551 and practolol in the concentrations given above. In this preparation the shift of the C/R curve of procaterol was ten times greater than that of isoprenaline after blockade with ICI 118,551, 10(-7) mol/l. We conclude that it is possible to characterize small fractions of beta 1-adrenoceptors coexisting with beta 2-adrenoceptors with the technique used. Furthermore there is still no functional evidence of the existence of beta 1-adrenoceptors in the lung parenchyma.

Adrenergic beta-Antagonists↗
PubMed1981

A comparison of the effects of sympathomimetic agents on gastric acid secretion by the rat stomach in vivo and in vitro.

1. The action of isoprenaline on gastric acid secretion in rats with Heidenhain pouches has been compared with its action in a rat isolated stomach preparation. 2. Isoprenaline (40 micrograms kg-1 h-1) inhibited the acid secretion in response to pentagastrin (20 micrograms kg-1 h-1) in conscious rate with Heidenhain pouches. 3. This inhibition could be abolished by propranolol (2 mg kg-1) and butoxamine (8 mg kg-1) and partially reversed by practolol (8 mg kg-1). 4. Propranolol (2 mg kg-1) significantly increased the response to pentagastrin (20 micrograms kt-1 h-1) but butoxamine and practolol (both at 8 mg kg-1) and the inactive isomer (+)-propranolol (2 mg kg-1) were without any effect on the pentagastrin response in the rats with pouches. 5. In the rat isolated stomach preparation isoprenaline stimulated acid secretion over the range 10(-7) M-10(-3) M whereas phenylephrine and methoxamine were without effect. 6. Propranolol (2 X 10(-5) M) inhibited this stimulatory effect of isoprenaline in vitro but (+)-propranolol (2 X 10(-5) M), practolol and butoxamine (both at 10(-4) M) had no effect on the response. 7. Propranolol (2 X 10(-5) M) did not have any effect on the response of the isolated stomach to pentagastrin (5 X 10(-7) M) or bethanechol (1.7 X 10(-5) M). 8. Phenylephrine (2 X 10(-5) M) did not affect the in vitro responses to pentagastrin (2.17 X 10(-7) M), bethanechol (1.7 X 10(-5) M) or histamine (5.4 X 10(-5) M). 9. It is concluded that isoprenaline has a direct stimulatory effect and an indirect inhibitory effect on gastric acid secretion in the rat. Both effects involve stimulation of beta-adrenoceptors. The relative predominance of one or other of these two opposing effects may help to explain the contradictory results in the literature regarding the actions of beta-adrenoceptor agonists on gastric acid secretion.

Adrenergic alpha-Agonists↗
PubMed1977

Hypothalamic action of adrenoreceptor blocking agents.

In cats anaesthetized with pentobarbital sodium, the posterior hypothalamus was superfused and electrically stimulated with a push-pull cannula. The pressor response to stimulation of this hypothalamic area was inhibited when the hypothalamus was superfused with drugs blocking either alpha-adrenoreceptors (piperoxan, tolazoline), or beta-adrenoreceptors--(+/-)-propranolol, (-)-propranolol, practolol, sotalol, metoprolol. (+)-Propranolol and a concentration of procaine equianaesthetic to propranolol were ineffective. During superfusion with tolazoline in the presence of practolol the inhibition was twice as that when the hypothalamus was superfused with either tolazoline or practolol. In another series of experiments the push-pull cannula was inserted into the anterior hypothalamus. The depressor response to stimulation of this area was inhibited by the hypothalamic superfusion with the alpha-adrenoreceptor blocking drugs phentolamine, tolazoline, piperoxan or yohimbine. Hypothalamic superfusion with phenylephrine abolished the inhibitory effect of phentolamine on the depressor response. The results indicate that adrenoreceptors are present in the hypothalamus and that they are involved in blood pressure changes elicited by hypothalamic stimulation.

Adrenergic alpha-Antagonists↗
PubMed1980

Stimulation by beta 2-adrenergic receptors of the production of cyclic AMP and progesterone in rat ovarian tissue.

Ovarian tissue from immature rats treated with pregnant mare serum gonadotrophin (PMSG) or PMSG and human chorionic gonadotrophin was incubated in Medium 199. Stimulation of the formation of cyclic AMP in follicular and luteal tissue by terbutaline (10(-5) mol/l), a selective beta 2-agonist, was blocked by butoxamine (10(-5) mol/l), a selective beta 2-antagonist, whereas practolol (10(-5) mol/l), a selective beta 1-antagonist, was ineffective. Propranolol (10(-5) mol/l) a non-selective beta-antagonist, butoxamine nor practolol affected the increase in cyclic AMP promoted by the addition of 1 microgram LH. Stimulation of the production of progesterone in both follicular and luteal tissue by terbutaline was blocked by butoxamine, but not by practolol. These findings indicated that beta-adrenergic stimulation of ovarian cyclic AMP and progesterone is mediated by beta 2-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1979

Tissue levels of several radiolabelled beta-adrenoceptor antagonists after intravenous administration in rats.

The uptake of radioactively labelled propranolol, oxprenolol, metoprolol, acebutolol, practolol and atenolol into brain, liver and lung tissue was studied five min after intravenous administration (1.0 mg/kg) in normotensive Wistar rats anaesthetised with nitrous oxide and halothane. All of the beta-adrenoceptor antagonists including the least lipophilic compounds atenolol and practolol were detected in brain tissue five min after systemic administration. However, the level of propranolol (as measured by total radioactivity) in the bran was 40 and 67 times greater than the levels found for atenolol and practolol, respectively. Additionally, significantly more radioactivity was detected in lung tissue compared to that in liver tissue for the lipophilic, non-selective beta-adrenoceptor antagonists propranolol and oxprenolol. Levels of radioactivity in blood, brain, liver and lung were measured 5, 15, 30 and 60 min after administration of either propranolol or atenolol (1.0 mg/kg, i.v.) to both conscious and anaesthetised rats and a tendency towards high tissue levels of radioactivity was found in the animals which received the beta-adrenoceptor antagonists under anaesthesia. Pretreatment of groups of rats for 7, 14 and 21 days with unlabelled atenolol (1.0 mg/kg/day, i.p.) caused an increase in the subsequent central uptake of labelled atenolol whilst both the blood levels of radioactivity and the uptake into peripheral tissues were significantly lower in the 2 and 3 week pretreated rats compared to the control animals. These results are consistent with the hypothesis that a central action may contribute to the antihypertensive effect of beta-adrenoceptor antagonists.

Adrenergic beta-Antagonists↗