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At least 613 records · Page 34Linked to original sources
PubMed1976

Interaction of anesthesia, beta-receptor blockade, and blood loss in dogs with induced myocardial infarction.

The cardiovascular effects of halothane-nitrous oxide anesthesia, and beta-receptor blockade with either propranolol or practolol, were studied in 15 dogs in which severe myocardial infarction had been induced ten days earlier. The hemodynamic responses to blood loss amounting to 25 per cent of estimated blood volume, and its subsequent replacement, were studied before and after induction of beta-receptor blockade. In terms of cardiac output and aortic blood flow acceleration, cardiac performance in the absence of beta-blockade was markedly impaired during steady-state anesthesia, compared with corresponding values in normal dogs. Practolol (2.0 mg/kg) administered during anesthesia induced no significant circulatory change other than a 14 per cent decrease in heart rate and a 25 per cent increase in strode volum. Propranolol (0.3 mg/kg) caused a comparable reduction of heart rate, but significantly reduced cardiac output (-27 per cent), aortic blood flow acceleration (-26 per cent), and peak LV power (-19 per cent), and increased systemic vascular resistance (+49 per cent). The two drugs caused comparable shifts of the isoproterenol dose-response curve during anesthesia. Graduated blood loss during anesthesia, to a total of 25 per cent of blood volume, caused consistent circulatory changes (decreased mean arterial pressure cardiac output, peak LV power, LV minute work) that were essentially similar before and after beta-receptor blockade with either propranolol or practolol. The positive inotropic effect of calcium gluconate during halothane anesthesia was significantly reduced following either propranolol or practolol, but the hemodynamic responses to changes of systemic vascular resistance induced with acetylcholine or phenylephrine were not modified by beta-receptor blockade.

Acetylcholine↗
PubMed1986

Adrenaline infusion evokes increased thromboxane B2 production by platelets in healthy men: the effect of beta-adrenoceptor blockade.

The effects of direct adrenergic stimulation, achieved by 60-min adrenaline infusion (0.1-0.2 microgram kg-1 min-1), on thromboxane B2 (TxB2) production by platelets in whole blood ex vivo and on ADP-induced platelet aggregation were studied in seven healthy male volunteers. The effects of two beta-adrenergic blocking agents, pindolol and practolol, on the adrenaline-induced changes were furthermore analyzed. Adrenaline administration resulted in an about ten-fold elevation in plasma adrenaline, and an about three-fold increase in TxB2 production by platelets at 30 min of infusion. The increased TxB2 production persisted throughout the entire adrenaline infusion, and up to 30 min of postinfusion period (recovery). Pindolol blunted markedly the effects of adrenaline on platelet TxB2 production, whereas practolol seemed to have only a weak effect. The sensitivity of platelets to ADP-induced aggregation did not change during the 60 min of adrenaline infusion. However, at 60 min of recovery the platelets showed a significantly increased sensitivity to ADP. Correspondingly, pindolol treatment did not affect platelet sensitivity during the infusion period, but at 60 min of recovery it had caused a significantly decreased sensitivity of platelets to ADP-stimulation. Plasma-free fatty acids increased markedly during the adrenaline infusion. This increase was totally blocked by pindolol, but only partly by practolol. The present results demonstrate that adrenaline, at plasma levels seen for example, in complicated myocardial infarction, stimulates platelet TxB2 production and increases the sensitivity of platelets to ADP after the infusion. Pindolol, but not practolol, inhibits these adrenaline-induced changes in platelet behaviour.

Adenosine Diphosphate↗
PubMed1975

Action of beta-adrenoceptor antagonists on the response to isoprenaline in the oestrogen dominated rabbit uterus.

1. Log dose-response curves to isoprenaline from spontaneously contracting muscle strips from rabbit uterus have been obtained. The effects of the alpha-adrenoceptor antagonists phentolamine and phenoxybenzamine, the beta- adrenoceptor antagonists propranolol and practolol, and (+)-propranolol on the log dose-response curves were studied. 2. Phentolamine 5.3 times 10- minus 7 M had a stimulating effect on the muscle strips, moving the log dose-response curve of isoprenaline to the right. Phenoxybenzamine 2.9 times 10- minus 5 M had no effect on the curves. 3. Propranolol 3.4 times 10- minus 6 M had no effect on the curves from circular muscle strips, with either phentolamine 5.4 times 10- minus 7 M or with phenoxybenzamine 2.9 times 10- minus 5 M as alpha-blocker. The curves from the longitudinal muscle strips were shifted somewhat to the right, the same shift, however, being obtained with (+)-propranolol 3.4 times 10- minus 6 M. 4. Practolol 3.8 times 10- minus 6, 3.8 times 10- minus 5 and 3.8 times 10- minus 4 M was without effect on the curves, either in the circular or in the longitudinal strips. 5. It is concluded that neither propranolol at 3.4 times 10- minus 6 M nor practolol act as beta-adrenoceptor antagonists in oestrogen dominated rabbit uterus. In all other tissues investigated, propranolol or practolol block the effect of isoprenaline. Whether the effect of isoprenaline in this tissue may be termed a beta-effect, is then a question of definition. In addition there is no evidence for any extraneuronal uptake mechanisms for isoprenaline. 6. Variations in sensitivity to beta-stimulation with the time of the year were observed, the sensitivity being greatest in the winter and lowest in the summer.

Adrenergic beta-Antagonists↗
PubMed1977

The selective action of beta-adrenoceptor blocking drugs and the nature of beta1 and beta2 adrenoceptors.

1 Purified membranes retaining a catecholamine responsive adenylate cyclase have prepared from rabbit heart, lung and (pseudo-pregnant) uterus. 2 These preparations have the characteristics of plasma membranes and both heart and lung respond to beta-adrenoceptor agonists in the order: (+/-)-isoprenaline greater than (-)-noradrenaline greater than (-)-adrenaline greater than (+)-isoprenaline greater than salbutamol. The sensitivity of the adenylate cyclase to beta-adrenoceptor stimulation is improved by pre-treatment of the animals with reserpine and syrosingopine. 3 Dose-ratios for several concentrations of propranolol (non-selective beta-adrenoceptor blocker), practolol and atenolol (cardio-selective beta-adrenoceptor blockers) have been measured on all three membrane preparations. Schild plots of log (dose ratio -1) vs. log dose were virtually coincident for heart and lung with a dissociation constant (Kb) for propranolol very close to the pharmacological value. The ratio of Kb values was 0.65 for practolol and 1.23 for atenolol compared with pharmacological cardio-selectivity ratios (measured on isolated atria and tracheal chain) of 67.6 and 110 respectively. The uterus/heart Kb ratio was 51.5 for atenolol. Inhibition of the uterus by practolol gave a Schild plot with slope significantly less than 1, indicating a different mechanism of action from the heart. 4 Kb values obtained by measuring adenylate cyclase stimulation in chopped tissue (including preparations of bronchial tree and alveolar tissue as well as whole lung) resembled the membrane values rather than those found in whole organs. 5 The results show that the pharmacological selectivity of practolol and atenolol is maintained at the receptor-adenylate cyclase level, at least as far as heart and uterus are concerned, though the smaller selectivity ratios in the biochemical system suggest that receptor differences is not the only factor and that phase distribution of the drug may also be important. Membranes prepared from whole lung show that phase distribution of the drug may also be important. Membranes prepared from whole lung show an overall beta1 response which may simply reflect the predominance of beta1 cell types containing beta1-adrenoceptors over bronchial smooth muscle.

Adenylyl Cyclases↗
PubMed1977

The uptake and overflow of radiolabelled beta-adrenoceptor blocking agents by the isolated vas deferens of the rat.

1. A comparison of uptake into and overflow from the isolated vas deferens of the rat has been made between [3H]-noradrenaline ([3H]-NA), [14C]-D-sorbitol and three radio-labelled beta-adrenoceptor blocking agents, [14C]-practolol, [14C]-(+/-)-propranolol and [3H]-penbutolol. 2. The accumulation of [3H]-NA after 30 min incubation was reduced by desmethylimipramine (DMI) 1 X 10(-8)M and was also reduced in vasa from rats pretreated with 6-hydroxydopamine (6-OHDA). This was not so with [14C]-D-sorbitol. 3. 6-OHDA pretreatment of the rats reduced the uptake of [3H]-penbutolol after 30 min incubation but not that of [4C]-propranolol or [14C]-practolol. DMI 1 X 10(-8)M did not alter the tissue uptake of [14C]-propranolol, [14C]-practolol or [3H]-penbutolol. 4. Electrical stimulation of vasa preloaded with [3H]-NA caused a significantly greater increase in [3H]-NA overflow than during the resting, unstimulated periods. No such increase in overflow was observed with [14C]-sorbitol or any of the three beta-adrenoceptor blocking agents use. 5. The beta-adrenoceptor blocking agent penbutolol was shown to possess adrenergic neurone blocking activity in the isolated vas deferens of the rat. 6. It is concluded that any effect that practolol or (+/-)-propranolol have on noradrenergic neurones is brought about without the need for these drugs to gain access to the interior of the neurone.

Adrenergic beta-Antagonists↗
PubMed1976

Effect of atenolol on ventilatory and cardiac function in asthma.

The effects on ventilatory and cardiac function of atenolol, a new cardioselective beta-adrenoceptor blocking agent, were compared with those of practolol in a double-blind trial in 12 patients with asthma. Both drugs impaired ventilatory function--atenolol insignificantly and practolol significantly. Atenolol was if anything more cardioselective than practolol. Neither drug interfered significantly with the bronchodilator response to inhaled isoprenaline. Atenolol is suitable for use in patients for whom practolol would formerly have been chosen because of its cardioselectivity.

Adrenergic beta-Antagonists↗
PubMed1977

Reduction in mortality after myocardial infarction with long-term beta-adrenoceptor blockade. Multicentre international study: supplementary report.

In a controlled multicentre trial carried out to assess the value of long-term practolol treatment after myocardial infarction the provisional results showed a significant reduction in mortality, though some of the data were lacking. These have now been included and the results updated. The final figures for all deaths were 78 in the placebo group of 1533 patients and 48 in the practolol group of 1520 patients. The reduction in mortality (38%) was significant at the 1% level. The figures for non-fatal reinfarction (97 in the placebo group, and 75 in the practolol group) were not significantly different. Patients with pre-entry anterior infarction, and especially those with a diastolic blood pressure equal to or below the mean (78 mm Hg) at entry to the trial, were at high risk but benefited particularly well from beta-adrenoceptor blockade. After pre-entry inferior infarction the percentage reduction in deaths occurring within two hours after symptoms of a new event was similar to that after anterior infarction, but the incidence of death more than two hours after the event was greater in the practolol-treated group. Thus the difference between groups in total deaths after pretrial inferior infarction was marginal. Until the results of further trials are reported long-term beta-adrenoceptor blockade (possibly up to two years) is recommended after uncomplicated anterior myocardial infarction.

Arrhythmias, Cardiac↗
PubMed1975

Effects of several beta-blockers on blood pressure in the rat.

Effects of practolol, alprenolol and pindolol on blood pressure in the rat were studied. Also effects of these three beta-blocking agents on blood pressure and heart rate in spinal rats during adrenaline infusion were studied and compared with those of propranolol. The beta-blocking agents produced a sustained pressor action in the rat, and in the spinal rat infused with adrenaline. The magnitude of the pressor action induced by the beta-blockers was in the following order: pindolol larger than or equal to propranolol larger than or equal to alprenolol greater than practolol. Minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline were in the following order; practolol greater than alprenolol larger than or equal to propranolol larger than or equal to pindolol. The magnitude of the pressor action produced by the same dose of these beta-blockers and minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline seemed to be roughly proportional to their beta-receptor blocking activities. It was concluded that the minimum doses of these beta-blockers required to cause a pressor action and the magnitude of the pressor action induced by the beta-blockers in the spinal rat infused with adrenaline could be used to compare their beta-blocking activities and that practolol, a cardioselective beta-blocker, seems to block not only cardiac beta-receptor but to some extent also peripheral vascular beta-receptors.

Adrenergic beta-Antagonists↗
PubMed1975

Effects of beta blockers on cardiac function and myocardial oxygen consumption in the isolated supported heart preparation of the dog.

Effects of 2 different types of beta blockers, CS-359 and practolol, on mechanical performance and myocardial oxygen consumption (MVO2) in the isovolumic contraction of the isolated, blood-perfused canine heart with a support dog were studied. Two dose levels of the beta blockers were given intravenously to the support dog, one of which was enough to produce a significant beta adrenergic blocking action and other of which was a higher dose to reveal a direct depressant action on the isolated heart. CS-359 in the lower dose produced significant decreases in heart rate (HR), peak ventricular systolic pressure (peak VSP), and peak dp/dt while practolol caused no change in these parameters. The HR of the support dog was significantly decreased to the same degree in the lower dose of respective blocker. In the higher dose CS-359 decreased all parameters more definitely whereas practolol diminished peak VSP and peak dp/dt but did not significantly HR. MVO2 was decreased dose-relatedly by CS-359, but not affected significantly by practolol. From the analysis of relationships of MVO2 to peak VSP and HR in the isolated heart it is concluded that the effective reduction in MVO2 by CS-359 resulted mainly from a reduction in the peak VSP in the lower dose and additional decrease in HR in the higher dose of CS-359.

Adrenergic beta-Antagonists↗
PubMed1977

Drug-induced sclerosing peritonitis.

The records and case reports of 20 patients presenting with practolol induced sclerosing peritonitis have been reviewed revealing striking similarities: symptoms and signs of bowel obstruction or the presence of a vague abdominal mass in a patient who is currently taking or has previously taken practolol should alert one to the possibility of sclerosing peritonitis as the cause. Skin or eye reactions attributed to practolol provide further strong support for the diagnosis. Although practolol has now been discontinued in New Zealand its effects may become manifest months or years later.

Colon↗
PubMed1985

Cardiac beta-adrenoceptor blockade: the quest for selectivity.

In the search for improved drugs much attention has been focussed on the need for greater selectivity of action. Knowing that all drugs are poisons, the pharmacologist must attempt to define the required effect more narrowly but remain aware of potential unwanted effects. These may come as a result of the primary pharmacological effect or be due to other properties of the drug molecule manifesting themselves in clinical use. This paper illustrates the process of drug discovery and development with special reference to beta-adrenoceptor antagonists. Starting from the role of noradrenaline in sympathetic transmission, many compounds have been synthesized with therapeutic aims in mind. From a series of bronchodilators, dichloro-isoprenaline emerged which unexpectedly blocked stimulation of beta-receptors. This compound proved unsatisfactory leading to the introduction of the first clinically successful beta-blocker, pronethalol. Concern about potential carcinogenic effects led to its being replaced by propanolol. Failure to recognise the full range of clinical contra-indications resulted in propranolol causing severe cardio-vascular and bronchial adverse reactions. Soon it was recognized that propranolol was a powerful local anaesthetic potentially acting as a myocardial depressant. More serious was the recognition that in certain circumstances high levels of sympathetic tone were an adaptive response to pathophysiological change and that interruption by beta-blockade was inevitably serious for the patient. Attempts to identify the properties responsible for unwanted effects directed attention to comparison with non-local anaesthetic water soluble compounds still retaining beta-blocking activity. One such compound, practolol, also proved to exhibit a higher affinity for beta-receptors in the heart than elsewhere leading to the concept of cardioselective beta-blockade. The pharmacology of this agent is reviewed but it proved to have unacceptable side effects in clinical use. The importance of practolol was to demonstrate that anginal relief was due to beta-blockade and not local anaesthetic activity. It also showed that cardiovascular adverse reactions and bronchospasm were significantly less common than with propranolol. However, in addition to being cardioselective, practolol also showed intrinsic sympathomimetic activity. This resulted in a smaller bradycardia at rest. Contrary to predictions this property did not prevent practolol becoming well accepted by both doctors and patients as an effective anti-anginal drug. It was the unrelated skin, eye and mucous membrane reactions which led to the compound being withdrawn.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Beta adrenoceptor control of the microvascular reserve in rabbit myocardium.

This study was performed to determine if the unperfused microvascular reserve in the rabbit heart can be controlled by beta adrenoceptors. Anesthetized, open chest rabbits (N = 54) were subjected to saline i.v., 0.7 mg/kg of atenolol i.v., 1 mg/kg of practolol, 0.1 microgram/kg of salbutamol, 1 microgram/kg of salbutamol or 0.7 mg/kg of atenolol + 1 microgram/kg of salbutamol treatments. In half these animals coronary flows were determined before and after treatment using radioactive microspheres. The others were given 100 mg/kg of fluorescein isothiocyanate-dextran and the hearts were removed and analyzed for perfused and total microvascular morphology. The fluorescence marked the perfused microvessels and the slides were stained to show all vessels. Control group blood flow was 213 +/- 25 ml/min/100 g. Flows decreased 25% with atenolol and practolol whereas no change was seen with salbutamol or atenolol + salbutamol. Total capillary volume fraction ranged from 0.15 to 0.20 mm3/mm3 with 60% of this perfused in controls. Atenolol significantly reduced this to 47% whereas practolol (90%), high-dose salbutamol (97%) and salbutamol + atenolol (99%) resulted in a significant mobilization. Low-dose salbutamol resulted in a mobilization of capillaries to a degree intermediate (79%) between controls and high-dose salbutamol. Total arteriolar volume fraction ranged from 0.002 to 0.004 mm3/mm3 and in controls 65% of this was perfused. This percentage was reduced with atenolol and significantly increased with all other treatments except practolol. Thus, blockade of beta-1 adrenoceptors results in decreases in the percentage of perfused microvessels whereas stimulation of beta-2 adrenoceptors results in an increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuterol↗
PubMedDate not supplied

Effect of cardiac beta-adrenergic blockade or denervation on cardiotoxicity of digoxin and an aminosugar cardenolide.

This study examined the role of cardiac beta-adrenergic receptors and cardiac sympathetic and vagal nerves in the cardiotoxicity of 3-beta-0-(4-amino-4,6-dideoxy-beta-D-glucopyranosyl) digitoxigenin hydrochloride (ASI-254). Vagally intact dogs received a constant rate intravenous infusion of either digoxin or ASI-254 in the presence and absence of practolol. Practolol pretreatment increased the dose of digoxin required to produce arrhythmias and markedly altered the pattern of toxicity, but did not alter the lethal dose. The terminal event was cardiac standstill rather than ventricular fibrillation as seen in digoxin control dogs. Practolol did not alter the toxic dose of ASI-254 and produced little change in the pattern of cardiotoxicity; both control and practolol-treated dogs died in cardiac standstill. Surgical sympathectomy did not alter the toxic dose of ASI-254, the character of toxicity, or the lethal dose compared to neurally intact dogs. However, vagal innervation may play a role in determining the type of cardiotoxicity produced by ASI-254. Vagotomy alone did not alter the toxic or the lethal dose of ASI-254; vagotomy did, however, alter the character of cardiotoxicity and terminal event. Our results indicate that ASI-254 infused intravenously does not interact with sites, central or peripheral, which activate the sympathetic nervous system. ASI-254 administered into the lateral ventricles produced signs of increased cardiac sympathetic nervous system activity. Tachycardia and arrhythmias produced by ICV ASI-254 appear to be neurally mediated since ganglionic blockade blunted these effects. These results suggest that ASI-254 is capable of interacting with central sympathetic nervous system structures, but in contrast to digoxin, access to these structures from intravenous administration is limited.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of beta adrenergic blocking drugs and trifluperidol on intestinal motility and splanchnic nerve activity in cats.

In cats anaesthetized with chloralose and urethane we studied the effect of the selective beta 1 adrenergic blocking practolol and the non-selective beta 1-2 adrenergic blocking pindolol on the intestinal motility, the efferent sympathetic activity, arterial blood pressure and heart-rate. We compared the effects of trifluperidol on the intestinal tone, the intestinal motility and its duration with those of trifluperidol and practolol combined. It was found that 1-, 2-, and 3 mg/kg of practolol given intravenously had no influence on the spontaneous electric activity of postganglionic fibres of the splanchnic or hypogastric nerves, thus it had no central effect. Accordingly, its site of effect proved to be peripheric. Its administration was associated with a slight decrease of the arterial blood pressure and heart rate. The intestinal tone was instantly increased depending on the does in every case. In two-thirds of our experiments the intestinal motility was restored 1 to 3 minutes following administration depending on the dose. Combined with trifluperidol, practolol produces a further increase in the enhancing activity of trifluperidol on the intestinal tone and motility. It considerably extends the duration of the action of trifluperidol on the intestinal motility. Pindolol increases the intestinal tone and motility dose-dependently in every case, reduces the efferent sympathetic activity, which is inversely proportional to the dose. The action is most pronounced on administration of 0.125 micrograms/kg of pindolol intravenously but it cannot be observed with a dose of 0.5 mg/kg. No significant changes were observed in blood pressure but there was a reduction in heart rate. The action of pindolol is supposed to be both central and peripheral in nature.

Animals↗
PubMed1976

Effects of cardioselective beta adrenoceptor blockade on specific airways resistance in normal subjects and in patients with bronchial asthma.

The effects of single oral doses of the cardioselective beta adrenoceptor blocking drugs, metoprolol and tolamolol, on specific airways resistance (SRaw) were compared with those of propranolol and practolol in 6 healthy volunteers and in 12 patients with bronchial asthma. Whole-body plethysmography was used to measure SRaw and the blocking potency of different antagonists assessed by the degree of inhibition of tachycardia due to exercise on a treadmill. The changes correlated with plasma drug levels. Propranolol and practolol were measured fluorometrically and metoprolol by electron-capture gas-liquid chromatography. In normal subjects, about 30% reduction in exercise-induced tachycardia resulted from single doses of 80 mg propranolol (plasma levels, 50.3, SD, 29.5 to 60.8, SD, 26 ng/ml), 250 mg practolol (plasma levels, 1.05, SD, 0.32 to 1.10, SD, 0.55 mug/ml), 100 mg metoprolol (plasma levels, 137, SD, 111 to 152, SD, 100 ng/ml), and 100 mg tolamolol. In patients, these doses of the drugs produced significant increases in SRaw. These increases were greater than those after placebo but significantly so only during the peak effect 1 hr after propranolol. Compared with changes after placebo, significant effects on SRaw were also found in 3 patients given 200 mg of tolamolol. None of the drugs had a significant effect on SRaw in normal subjects. It is concluded that metoprolol, practolol, and tolamolol may impair ventilatory function in asthmatics less than propranolol and that at high doses this difference may not be demonstrable.

Adrenergic beta-Antagonists↗
PubMed1979

[Effects of four beta-blocking agents on some psychopharmacological tests in mice (author's transl)].

Common effects of four beta-adrenergic blocking drugs have been investigated in mice using classical and new psychopharmacological tests. Propranolol, alprenolol, practolol and penbutolol reduced the increase in locomotor activity produced by reserpine after MAO inhibition; they produce hypothermia when associated with amphetamine and they increase oxotremorine-induced hypothermia. Regarding these three tests the studied substances ranged themseleves in the same order of potency: penbutolol greater than propranolol greater than alprenolol greater than practolol. Propranolol and penbutolol decreased the toxicity provoked in crowded mice by amphetamine or by the association pargyline-reserpine; alprenolol and practolol did not. Propranolol, penbutolol and alprenolol antagonized the amphetamine-induced increase in motor activity; practolol did not. When used at doses for which d-l propranolol was active, the dextrogyre isomer of propranolol was without effect whatever the test studied. It is suggested that for the selection of a beta-blocking drug, regarding central effects in man, the tests described would deserve consideration.

Adrenergic beta-Antagonists↗
PubMed1994

Noradrenaline-serotonin interactions in the anxiolytic effects of 5-HT(1A) agonists.

The purpose of this study was to analyse adrenergic and serotonergic interactions in the anxiolytic effects of several 5-HT(1A) agonists including ipsapirone, buspirone, indorenate and 8-OH-DPAT. To this end, the effects of different doses of the adrenergic compounds clonidine (0.015-0.0625mg/kg), yohimbine (0.125-0.5mg/kg), prazosin (0.5-2.0mg/kg), pindolol (1.55-6.2mg/kg) and practolol (0.25-1.0mg/kg) on defensive burying behaviour were established. Clonidine (0.015-0.0625mg/kg), prazosin (1.0 and 2.0mg/kg), pindolol (1.55 and 6.2mg/kg) and all 5-HT(1A) agonists reduced burying behaviour by themselves. In contrast, yohimbine (0.250 and 0.5mg/kg) increased, while practolol did not modify, this behaviour. Additionally, the actions of yohimbine (0.125mg/kg), prazosin (0.5mg/kg), pindolol (3.1mg/kg) and practolol (0.5mg/kg) on the effects of ipsapirone (5.0mg/kg), buspirone (5.0mg/kg), indorenate (5.0mg/kg) and 8-OH-DPAT (0.25mg/kg) were examined. Prazosin enhanced the effects of ipsapirone, indorenate and buspirone, while yohimbine antagonized the actions of indorenate and 8-OH-DPAT. Pindolol enhanced the effects of indorenate while practolol antagonized the actions of ipsapirone, buspirone and 8-OH-DPAT. Only buspirone (5.0mg/kg) affected motor coordination, an effect that was not counteracted by the antagonists. Based on these data an interaction between 5-HT(1A) agonists and the noradrenergic system in the regulation of anxiety is proposed.

Journal Article↗
PubMed1972

Comparative study of six -adrenoceptive antagonists on airway resistance and heart rate in the guinea-pig.

1. The effects of six beta-adrenoceptive antagonists [(+/-)-propranolol, (+)-propranolol, (+/-)-sotalol, (+/-)-practolol, (+/-)-pindolol and (+/-)-procinolol] were studied on airway resistance and heart rate in guinea-pigs and dose-response curves constructed.2. All beta-adrenoceptive antagonists decreased heart rate and increased airway resistance. A significant correlation was found between the increase in airway resistance and the degree of bradycardia induced by all drugs except practolol. The orders of activity of the six drugs in inducing significant variations of the two parameters were respectively, for airway resistance: (+/-)-procinolol>(+/-)-pindolol>(+/-)-propranolol>(+/-)-sotalol>(+)-propranolol>(+/-)-practolol, and for heart rate: (+/-)-pindolol>(+/-)-procinolol>(+/-)-propranolol>(+/-)-sotalol>(+)-propranolol>(+/-)-practolol.3. (+/-)-Sotalol, (+/-)-pindolol and (+/-)-procinolol-induced changes in airway resistance and heart rate reached plateau values, which were not modified by increasing the dose. Since sotalol and procinolol have only very weak partial agonist and cardiac depressant properties, it appears that these changes can mainly be accounted for by the suppression of sympathetic tone. It is probable that this is also the case with pindolol.4. On the other hand, (+/-)-propranolol and (+)-propranolol induced dose-related changes in airway resistance and heart rate. Thus, a direct and non-specific effect of both drugs on the bronchial muscle, similar to that observed on the heart appears to be implicated, together with sympathetic tone suppression in these variations.5. (+/-)-Practolol-induced effects on airway resistance and heart rate were different from those observed with the five other beta-adrenoceptive antagonists.

Acetanilides↗