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PubMedDate not supplied

The effect of adrenaline on acetylcholine synthesis after blockade of alpha- and beta-adrenergic receptors in vitro.

The aim of the present work was to explain the mechanism of the stimulating effect of adrenaline (A) on acetylcholine (ACh) synthesis. This action is exerted most probably through the beta- adrenergic receptors, since propranolol and oxprenolol inhibit the stimulating effect of adrenaline on acetylcholine synthesis in the rat cerebral cortex in vitro. Dihydroergotamine does not show such effect. Practolol and phentolamine decrease the spontaneous synthesis of ACh in concentration several times lower than that inhibiting the ACh synthesis stimulated by adrenaline. It is suggested that adrenaline-induced stimulation of ACh synthesis in the rat cerebral cortex is not due to cyclic AMP, because noradrenaline (NA) does not increase ACh synthesis either in vivo or in vitro, although it activates the adenyl cyclase. NA on the other hand activates ACh synthesis in the calcium-free medium, which inhibits activating effect of NA on adenyl cyclase. Moreover it was found that cyclic AMP depresses ACh synthesis in the rat cerebral cortex in vitro.

Acetylcholine↗
PubMed1975

[Comparative evaluation of new drugs used in the treatment of cardiac arrhythmia].

The paper summarizes the experience gained in treating 830 patients with various cardiac rhythm disorders by employing new antirhythmic agents (propranolol, practolol, pindolol, alprenolol, oxyprenolol, benzoral, verapamil, lidocaine, imaline, sparteine, pulsonorma, disopyramide and quinidine durules). Comparative data on the efficacy of these agents are presented and indications and counterindications for their use are discussed.

Administration, Oral↗
PubMed1975

A comparative study of the activity of beta-adrenoceptor antagonists in man.

1. In healthy subjects the plasma concentration of unchanged drug, heart rate response to excerise and attenuation of isoprenaline tachycardia were maximal at one hour after ingestion of a range of doses of propranolol, oxprenolol, practolol, tolamolol, atenolol and metoprolol. 2. There was a within-drug relationship between plasma concentration of unchanged drug and the attenuation of exercise and iosprenaline tachycardia. There was no similar between-drug relationship. 3. There was a similar exponential relationship between oral dose and reduction of exercise tachycardia for all six drugs. 4. The linear relationship between oral dose and antagonism of infused isoprenaline was significantly greater for oxprenolol and propranolol than for the other four drugs. 5. "Cardioselective" activity was the only ancillary pharmacological property which differentiated the activity of these drugs in normal subjects.

Adrenergic beta-Antagonists↗
PubMed1976

Central regulation of blood eosinophilia by the beta-adrenergic system in rats.

The effect of isoprenaline and three different beta-adrenergic blocking agents on blood eosinophilia was evaluated in the rat. Eosinopenic effect of isoprenaline was antagonized by intraperitoneal pretreatment with propranolol and by high but not low doses of practolol. Sotalol, a beta-blocker which in contrast to propranolol does not penetrate the blood-brain barrier, did not affect the eosinophil count when injected intraperitoneally, but produced a marked increase in number of circulating eosinophils following intracerebroventricular injection. Intraperitoneal administration of isoprenaline and propranolol as well as intracerebroventricular injection of sotalol did not affect eosinophil count in adrenalectomized or hypophysectomized rats. These results suggest that beta-adrenergic agents regulate the number of circulating eosinophils through a central mechanism and that presence of both hypophysis and adrenal glands is required for this action.

Adrenalectomy↗
PubMed1989

Effects of selective and non-selective beta 1-blockade on renin secretion in the isolated rat kidney.

The participation of beta 1-adrenoceptor on renin secretion was studied in perfused rat kidney. Administration of propranolol, inhibited the renin release mediated by isoproterenol. Likewise, metoprolol and practolol, showed a similar potency to propranolol in inhibiting isoproterenol-induced renin secretion. These results suggest that the for isoproterenol-induced renin release in rats is a beta 1-type adrenoceptor.

Adrenergic beta-Antagonists↗
PubMed1978

Inhibition of thermogenic drinking by beta-adrenergic antagonists.

The thirst induced by transfer of rats from air at 5 degrees C to air at 25 degrees C (thermogenic drink) was inhibited by d,1-, but not d-propranolol (6 mg/kg body weight) administered 0.5 h prior to removal from cold. The thermogenic drink was not inhibited by a similar administration of the beta1-adrenergic antagonist, practolol (50 and 150 mg/kg body weight), but was inhibited by the beta2-adrenergic antagonist, butoxamine (35 mg/kg body weight). The results are consistent with the suggestion that beta2-adrenergic receptors play a role in mediation of the thermogenic drink in rats.

Adrenergic beta-Antagonists↗
PubMed1987

Influence of sympathetic withdrawal on early postinfarction arrhythmias.

In this work we studied the incidence and characteristics of early postinfarction arrhythmias in rabbits with sympathetic denervation. The electrical and haemodynamic changes were analyzed. Three groups of animals submitted to coronary occlusion were studied. A control group of normal animals (I), another group of animals injected with practolol prior to occlusion (5 mg/kg i.v.) (II) and a third group of animals in which stellate ganglia were surgically excised prior to occlusion (III). In the control group incidence of early postinfarction arrhythmias was 60% (12 of 20) while in Groups II and III incidence was only 25% (3 of 12 rabbits). The influence of excision or pharmacological blockade of sympathetic system and their role in the genesis of the early arrhythmias is discussed.

Animals↗
PubMed1985

Comparative response of 2-week and 6-month old rat myocardium to hypoxia.

The effect of hypoxia on contractile performance of left ventricular papillary muscles from 2-week old and 6-month old rats was studied. Left ventricular glycogen concentration was not significantly different between 2-week and 6-month old hearts; however, the lactate dehydrogenase isoenzyme pattern of the left ventricular myocardium from the 2-week old rats demonstrated a shift toward M-type (anaerobic) distribution relative to 6-month-old animals. Papillary muscle performance was studied at 28 degrees C while contracting 12 times/min at the peak of the active tension curve in oxygenated (95% oxygen, 5% carbon dioxide) Krebs-Henseleit solution containing glucose concentrations from 5.5 to 22 mM. In a bath containing 5.5 mM glucose, the decline in developed tension during hypoxia (95% nitrogen, 5% carbon dioxide) of preparations from the 2-week old rats was significantly less (P less than 0.05) than the 6-month old group only at 15 min. Raising the glucose concentrations of the bath to 11 and 16.5 mM resulted in improved performance throughout 60 min of hypoxia in preparations from 2-week compared with 6-month old animals. Practolol (5 X 10(-5)M) did not prevent the increased tolerance to hypoxia observed in preparations from 2-week animals. Thus, increasing anaerobic substrate has differential effects on the performance of 2-week and 6-month myocardium during hypoxia. The data suggests that in contrast to 6-month old heart muscle, myocardium from 2-week old rats is capable of modulating its active mechanical activity during hypoxia in accordance with the availability of glycolyptic substrate.

Adrenergic beta-Antagonists↗
PubMed1985

Beta-adrenergic receptor subtypes and subcellular compartmentation of cyclic AMP and cyclic AMP-dependent protein kinase in rabbit cardiomyocytes.

In purified ventricular myocytes from adult rabbit, beta-adrenergic stimulation causes cyclic AMP accumulation and cyclic AMP-protein kinase activation in both particulate and soluble fractions of the cell, whereas prostaglandin E1 elevates cyclic AMP and cyclic AMP-protein kinase activity in the soluble fraction exclusively. Only activation of particulate cyclic AMP-protein kinase activity results in phosphorylase b----a conversion. Using radioligand binding technics, we have determined whether beta 1- and beta 2-receptor subtypes mediate beta-adrenergic effects in particulate and soluble subcellular compartments, respectively. The non-selective antagonist [125I]iodocyanopindolol binds to intact ventricular myocytes with KD of 25 pM and a Bmax of 2.6 X 10(5) receptors/myocyte. Competition for [125I]iodocyanopindolol binding to intact myocytes by the beta-receptor subtype-specific antagonists practolol (beta 1) and zinterol (beta 2) results in monophasic curves with antagonist KD values of 1 microM and 1.5 microM, respectively. We conclude that adult rabbit cardiac myocytes do not possess detectable beta 2 receptors. Further, the ability of isoproterenol to cause elevation of cyclic AMP in two functionally distinct regions within the myocyte must pertain to the actions of a single subtype of beta-receptor, the beta 1-receptor.

Alprostadil↗
PubMed1987

Beta-adrenergic receptors in human trabecular meshwork. Identification and autoradiographic localization.

Beta-adrenergic receptors were identified in slide-mounted sections of human trabecular meshwork by in-vitro labeling, light microscopic autoradiography. Autoradiograms were generated after incubation of slide-mounted tissue sections with 125I-cyanopindolol, a selective high-affinity probe for beta-adrenergic receptors. Experiments in which an excess of either unlabeled Practolol (beta 1 selective ligand) or Zinterol (beta 2 selective ligand) were included suggested that most of the receptors were of the beta 2 subtype. Data from displacement studies using increasing concentrations of the highly specific beta 1- and beta 2-adrenergic receptor antagonists, ICI-89,406 and ICI-118,551, respectively, confirmed the predominance of the beta 2-adrenergic receptors. Similar results obtained with cultured trabecular endothelial cells suggest that the beta-adrenergic receptors may be associated with the endothelial cells of the trabecular meshwork in vivo. These results provide anatomic evidence for the hypothesis that beta-adrenergic agents improve outflow by direct action on the trabecular meshwork and provide a rationale for the development of more selective beta 2-adrenergic agents to increase outflow facility.

Autoradiography↗
PubMed1977

Ocular effects of beta-blocking therapy.

A survey of 192 patients receiving beta-blocking drug therapy has been carried out. An ophthalmological examination was performed on each patient with particular reference to the clinical status of the cornea and conjunctiva, and to lacrimal function. A selected control group of 52 patients was similarly investigated. The results indicate that the beta-blocking drugs administered to the survey group did not produce any significant adverse effect on the cornea, conjunctiva, or tear secretion when compared with the control group. The findings did not provide any evidence to incriminate the non-practolol beta-blocking agents with the production of ocular pathology.

Adrenergic beta-Antagonists↗
PubMed1979

[Effects of beta blockaders on ventilatory function in chronic bronchitis].

This study was carried out to determine whether beta blockers could be prescribed for patients with coronary insufficiency and chronic bronchitis. The effects of intravenous infusions (30 mn) of propranolol (30 micrograms/kg), practolol 90 micrograms/kg), atenolol (90 micrograms/kg) and acebutolol (150 micrograms/kg) on vital capacity and expiratory flow rates were investigated in chronic bronchitics. Propranolol (n = 51) moderately reduced the vital capacity and FEV1, by an average 9% and a maximum of 20%. The three other infused agents given to groups of 10 patients did not change the ventilatory function. When the same patients were investigated by cross over with propranol bronchoconstriction was observed. This effect was seen in all stages of chronic bronchitis but was much less severe than in a group of 50 asthmatic patients (-23%). The respiratory tolerance of the cardioselective beta blockers seems to be better but there is considerable individual variation and the diagnosis between asthma and chronic bronchitis may itself be very difficult.

Acebutolol↗
PubMed1978

Influence of digitalis on cardiac function before and after autonomic blockade.

The influence of Deslanoside C (D), 1.2 mg intravenously on the systolic time intervals (STI) was assessed in 15 individuals with right ventricular pacemakers, who were studied on two occasions, ten days apart. In the first case D was given under basal conditions, and in the second after autonomic blockade (with practolol 20 mg intravenously and atropine 1.5 and 1.0 mg intravenously) at 1 hour's interval. There were similar changes of the STI with digitalis administration both before and after automic blockade. Autonomic blockade is not necessary for full expression of digitalis action on the human heart, as advocated by some authors to be the case in experimental animals.

Adult↗
PubMed1979

[Cutaneous reactions to propranolol (author's transl)].

A 17-year-old male patient with eczematous and psoriasiform eruption that developed during long-term therapy with Propanolol (Avlocardyl) has been studied. This eruption disappeared after removal of the drug; oral challenge was soon followed by a vesiculous and bullous eruption of face and extremities; five months later, sun exposure was followed by a severe eczematous eruption in these areas; nails changes were then observed. Most of side-effects of beta-adrenergic blocking drugs have been reported with Practolol: lichenoid, exanthematous, eczematous, psoriasiform rashes; exfoliative dermatitis; oculo-muco-cutaneous reactions; fibrosing polyseritis and drug induced systemic lupus erythematosus manifestations. Adverse effects of other beta-adrenergic blocking agents are less frequent. The pathogenetic mechanism responsible for these adverse reactions is still obscur: these changes might be caused by blockade of the epidermal cells (and T-lymphocytes) beta-receptors, more than by a direct immunologic, allergic or toxic mechanism.

Adolescent↗
PubMed1979

Effects of 4 beta-adrenoceptor blocking drugs on blood pressure and exercise heart rate in hypertension.

The effects of 4 beta-adrenoceptor blocking drugs on blood pressure and on exercise tachycardia were compared in a within-patient study of patients with uncomplicated essential hypertension. Twelve patients were treated with propranolol, practolol and atenolol and 7 of the same patients also received oxprenolol. Each patient received each drug separately, withdrawing each drug before starting the next, and each patient was titrated to the lowest attainable blood pressure and heart rate with each compound. All 4 drugs caused reductions in both systolic and diastolic blood pressure and in the heart rate induced by exercise. The maximum reduction by each drug in both systolic and diastolic blood pressure was the same. There were small but significant differences in the effects on heart rate between those drugs which had intrinsic sympathomimetic activity and those which did not have this property.

Adrenergic beta-Antagonists↗
PubMed1979

Rate of pressure change and hyperbaric bradycardia in the mouse sinus node.

Sinus node preparations from mice were hydraulically compressed at 10, 100, and 500 atm x min-1 in Tyrode's solution at 27 degrees C. At the highest compression rate, both a delay and a more pronounced beating frequency response to pressure was seen. The delayed reaction is ascribed to either adiabatic effects or a time-delay in conformational changes in the pacemaker cell membrane. The potentiating effect of a high compression rate could be eliminated by autonomic blockade (atropine and practolol).

Animals↗
PubMed1977

[Insulin-poietic effect of pentagastrin after beta-adrenergic block in the anesthesized dog].

Infusion of pentagastrin (5-G) into the femoral vein of anaesthesized dogs, in doses of 0.20 microgram/kg/min for 30 minutes, causes a prompt and significant increase in plasma IRI. The insulin-secretory effect of the peptide was not affected by 0.5 mg/kg i.v. of propranolol (a beta-adrenergic blocking agent) or by 1.3 mg/kg i.v. of practolol (a selective beta1-adrenergic blocking agent). These results show that the action of 5-G on the pancreatic beta-cells could be not related to the beta-adrenergic system.

Anesthesia↗
PubMed1980

[Quantitative morphologic studies on the myocardium in early stages of ontogenesis and after application of various cardioactive agents].

The authors have morphometrically studied the differentiation of the myocardium in dynamic phases of the embryonic and postnatal development in chickens and Syrian Hamsters. Moreover, they investigated the action of the beta-adrenalytic substances Practolol and Trimepranol on ultrastructure of the cardiac muscle in adult animals. The volume of mitochondria in myocardial cells in 6-day old chicken embryos amounts to 5.65% of the total cell volume, in 12-day old embryos 14.35%, in 18-day old embryos 19.60%, in 1-day old chickens 23.24% which is nearly as much as in adult animals. The volume of myofibrils in 6-day old embryos is about 3.2%, in 12-day old embryos about 7.4%, in 18-day old embryos about 16.4% and in 1-day old chickens about 21.2%. The differences between individual groups are statistically significant. The dynamics of differentiation of the myocardium in Syrian Hamsters was studied in 5 phases, namely in 14-day old embryos and in postnatal phases on the 2nd, 5th, 14th and 21st days after birth. Most cells in 14-day old embryos are rather immature. Participation of the volume of mitochondria, myofibrils, equipment of mitochondria with cristae etc. considerably increase in postnatal phases. These findings suggest that the heart of mammals is rather immature at birth and will differentiate mainly in the postnatal developmental phases. Many morphometric findings, as regards the action of beta-adrenalytic drugs on the ultrastructure of the myocardium in adult rabbits, point to the fact that application of these substances will give rise to degenerative alterations in approximately 10% of myocardial cells. Theoretical explantation of these mechanisms is being discussed.

Animals↗