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PubMed1985

Comparison of beta-adrenoceptor populations in cat and guinea-pig left atria.

The subtypes of beta-adrenoceptor present in left atrial preparations from the guinea-pig and cat have been assessed using both responses obtained in organ bath experiments and radioligand binding studies. From the positive inotropic responses to procaterol, the pKB values for practolol using a variety of agonists, and from displacement of [125I]cyanopindolol from left atrial membrane homogenates by the selective beta 1- and beta 2-adrenoceptor antagonists L643,717-01J10 and ICI 118,551, it was concluded that guinea-pig left atria possess only beta 1-adrenoceptors, whilst cat left atria possess both beta 1- and beta 2-adrenoceptor subtypes.

Adrenergic beta-Antagonists↗
PubMed1985

Homogeneity of beta-adrenoceptors on bovine teat muscles.

Bovine teat beta-adrenergic receptors were investigated with binding studies using 3H-dihydroalprenolol (DHA) as ligand. Inhibition of 3H-DHA-binding by beta 1-(betaxolol, atenolol, practolol) and beta 2-(zinterol, fenoterol, ICI 118551) selective drugs resulted in monophasic displacement curves with Hill coefficients close to 1.0. Computer assisted analysis of these curves did not reveal the presence of more than one class of binding sites. These data suggest that the beta-receptor sites present in bovine teat walls are of the beta 2-subclass.

Adrenergic beta-Antagonists↗
PubMed1985

Cholinergic involvement in the modulation of oxotremorine-tremor in mice by propranolol.

Propranolol in low doses antagonized and in higher doses facilitated oxotremorine-induced tremor (Oxo-tremor) in mice. Atropine blocked Oxo-tremor, an effect that was reversed by propranolol. Atropine pretreatment also antagonized the potentiating effect of propranolol on Oxo-tremor. Propranolol inhibited mice brain cholinesterase at doses which enhanced Oxo-tremor. Timolol and sotalol produced a dose-dependent antagonism of Oxo-tremor, whereas practolol failed to produce a similar effect. None of these three agents produced any significant enhancement of Oxo-tremor. These results suggest the involvement of a peripheral mechanism for the antagonism and a central cholinergic mechanism for the facilitation of Oxo-tremor by propranolol.

Adrenergic beta-Antagonists↗
PubMed1986

Ablation of the myenteric plexus impairs alpha but not beta adrenergic receptor-mediated mechanical responses of rat jejunal longitudinal muscle.

The mechanical responses produced by alpha and beta adrenergic receptor agonists were evaluated in control and myenteric neuron-ablated rat jejunal longitudinal muscle. The myenteric plexus of the jejunum was destroyed by serosal application of benzalkonium chloride (BAC). The beta adrenergic receptor agonists isoproterenol and sulfonterol produced a concentration-dependent relaxation of both control and BAC-treated jejunum. Dose-response curves obtained in control and BAC-treated jejunum were nearly superimposable regardless of the beta agonist used. Isoproterenol-induced relaxation was antagonized by the beta receptor antagonists propranolol and practolol but not by butoxamine. The alpha-1 selective agonists phenylephrine and methoxamine were more potent and efficacious in producing relaxation of control than BAC-treated jejunum. The relaxant responses of methoxamine and phenylephrine in control jejunum were blocked by prazosin but not by yohimbine. The supposed alpha-2 selective agonist clonidine also produced a concentration-dependent, prazosin-sensitive, yohimbine-resistant relaxation which was markedly greater in control than BAC-treated jejunum, consistent with alpha-1 receptor stimulation. Clonidine tested in the presence of prazosin and the alpha-2 selective receptor agonists UK-14,304, M-7 and B-HT 920 all produced a concentration-dependent contraction of control but not BAC-treated jejunum. The contractile response produced by UK-14,304 was antagonized by yohimbine but not by atropine. Our results suggest that in rat jejunal longitudinal muscle: beta adrenergic receptors mediate relaxation and are located on the smooth muscle; alpha-1 adrenergic receptors mediate relaxation and are located on both the smooth muscle and myenteric plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

In vitro effects of beta adrenoceptor agonists and antagonists on the rat ovarian suspensory ligament.

The mesovarian suspensory ligament of the rat was used to compare the activities of beta adrenoceptor agonists and antagonists. The following beta adrenoceptor agonists, in descending order of potency, inhibited spontaneous activity in a dose-related manner: zinterol greater than isoproterenol much greater than dobutamine. Several noncardioselective, beta-2 adrenoceptor antagonists with intrinsic sympathomimetic activity (ISA) also inhibited the activity of the ligament: pindolol greater than alprenolol = bucindolol = oxprenolol greater than labetalol. Maximal relaxation induced by the antagonists was equivalent to that caused by the beta receptor agonists. Two cardioselective, beta adrenoceptor antagonists with ISA, acebutolol and practolol, did not inhibit the activity of the suspensory ligament but did increase the rate of the isolated right atrium of the rat. The maximal increases in atrial rate evoked by the antagonists were significantly less than those induced by the beta adrenoceptor agonists. Studies with ICI 118,551 or atenolol as beta-2 or beta-1 selective adrenoceptor blockers, respectively, suggest that the beta adrenoceptors of the suspensory ligament are predominantly of the beta-2 subtype. The possible relevance of these results to the induction of mesovarian leiomyomas in rats by noncardioselective beta adrenoceptor agonists and antagonists with ISA is discussed.

Adrenergic beta-Agonists↗
PubMed1987

Interaction of beta adrenergic agonists and antagonists with brain beta adrenergic receptors in vivo.

There is interest in knowing whether beta adrenergic antagonists or agonists, when administered systemically, can enter the brain to interact with central beta adrenergic receptors. To study this, the reduction in the radioactive content in the brain of rats after administration of (-)-[125I]iodopindolol (IPIN) by systemically administered beta agonists or antagonists was measured. Previous studies show that after the i.v. administration of IPIN the binding in vivo to various areas of the central nervous system has the characteristics expected of binding to beta adrenergic receptors. Of the antagonists tested, pindolol and butylpindolol showed potent interactions with beta receptors in both cortex and cerebellum whereas atenolol and practolol did not interact at doses up to 30 mg/kg. CGP-12177 showed moderate potency in inhibiting IPIN binding in vivo. We have shown previously that propranolol and alprenolol inhibit IPIN binding with high potency in cortex and cerebellum. At high doses, butoxamine, a beta-2 antagonist, reduced the binding of IPIN in the cerebellum but not in the cortex. Of the agonists tested, clenbuterol and prenalterol caused a significant dose-dependent reduction of the binding of IPIN, with clenbuterol being more potent. Isoproterenol, salbutamol, salmefamol and dobutamine had no effect. With the exception of CGP-12177, the affinity of the drugs for central beta adrenergic receptors measured in vitro was correlated significantly with their ability to inhibit IPIN binding in vivo whereas their degree of lipophilicity was not correlated significantly with potency in vivo. The inhibition of IPIN binding in vivo from brain areas can be used to evaluate whether drugs penetrate into brain and interact with central beta adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1988

Beta-blockage therapy and cardiovascular disease. Past, present, and future.

The concept of two patterns of catecholamine activity was first described at the turn of the century by Langely and Dale. In the late 1940s, Ahlquist conceptualized the alpha- and beta-blocking actions of catecholamines. Sir James Black's research in the 1950s led to the introduction of pronethalol and then of propranolol into the therapeutics of angina and arrhythmias. Early beta-receptor blocking compounds were noted not only to be competitive inhibitors of the beta receptor but to have a direct depressant, membrane-stabilizing action. Later compounds, such as pindolol, were noted to have partial agonist activity. Practolol, metoprolol, atenolol, and similar "cardioselective", or beta-selective, drugs were subsequently described. Agents that combine beta blockade with alpha blockade or vasodilator action have been developed recently. There are various therapeutically advantageous pharmacodynamic differences among the beta-blocking drugs, such as less effect of beta 1-selective drugs on bronchial smooth muscle. Lipid solubility, systemic bioavailability, first-pass liver metabolism, renal excretion, and brain penetration are pharmacokinetic properties that further distinguish one agent from another. After the initial predicted therapeutic uses, beta-blocking drugs were used in hypertension and subsequently have been applied in a wide range of cardiovascular conditions. Recent work clearly demonstrating a cardioprotective effect in the post-myocardial infarction period is a major reason that use of the agents is likely to remain high.

Adrenergic beta-Antagonists↗
PubMed1978

[Effects of a new beta-blocker (CI 775) on left ventricular hemodynamics at rest and during exercise (author's transl)].

The effects of a new beta-blocking agent (CI 778) were studied in 8 patients in whom non-invasive data suggested absence of significant organic heart disease. The left ventricular hemodynamics at rest and during bicycle exercise were measured before and after intravenous administration of 0,9 mg/kg body weight. With exercise there was a significantly smaller increment of heart rate (18%) after beta-blockade. Stroke volume index at rest was significantly lower (17%) after administration of CI 775; the difference disappeared with exercise. There was an 18% decrease of the resting cardiac output after CI 775 and a 23% decrease with exercise. Significant changes at rest and with exercise indicating a negative inotropic action of CI 775 were noted for max dP/dt and peak measured velocity of circumferential fiber shortening (Vpm). The left ventricular enddiastolic pressure with exercise increased with borderline significance by 41% after CI 775. Also left ventricular stroke work index at rest and with exercise decreased moderately (n.s.), the systemic arterial resistance changed to the same extent as cardiac output decreased. Also the arterial venous oxygen difference increased after CI 775 only according to the decrease of cardiac output. The data suggest the hemodynamic properties of CI 775 are located between propranolol and practolol within the spectrum of available beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1977

Effect of propranolol on platelet function.

Excessive reactivity of blood platelets may contribute to atherosclerotic vascular disease. Hence drugs which alter platelet function may be protective. Prompted by findings that propranolol therapy normalized hyperactive platelet aggregation in patients with coronary artery disease, we studied propranolol in vitro to assess its action on platelets. At concentrations similar to those achieved in vivo (0.1-1 muM), propranolol raised the thresholds for aggregation of some normal paltelets by adenosine diphosphate (ADP). At higher concentrations (10-50 muM), propranolol abolished the second wave of platelet aggregation induced by ADP and epinephrine, and inhibited aggregation induced by collagen, thrombin, and the ionophore A23187. Propanolol blocked the release of 14C-serotonin from platelets, inhibited platelet adhesion to collagen, and interfered with clot retraction. Propranolol blocked ionophore-induced uptake of 45Ca by platelets. Inhibition appeared unrelated to beta-adrenergic blockage, as d(+) propranolol (which lacks beta-blocking activity) was equipotent with 1(-) propranolol. Moreover, practolol, a beta-blockading drug which is nonlipophilic, did not inhibit platelet function. These studies suggested that propranolol, like local anesthetics, decreased platelet responsiveness by a direct action on the platelet membrane, possibly by interfering with calcium availability. Modulation of platelet function by propranolol may occur at concentrations achieved at usual clinical doses of the drug.

Blood Coagulation Tests↗
PubMedDate not supplied

Uptake and displacement of [3H]-propranolol and [3H]-chlorpromazine in isolated, recirculating perfused guinea-pig lungs.

The pulmonary uptake of tritium labelled propranolol and chlorpromazine and their displacement by amphiphilic drugs has been studied in isolated guinea-pig lungs. Lungs were perfused by recirculation with 60 ml tyrode solution (carbogen gassed, 37 degrees C, 6% hydroxy-ethyl-starch) at a flow rate of 10 ml/min. In uptake experiments, a steady state was reached within 20 min with 95% of 10(-9) M propranolol and 90% of 10(-9) M chlorpromazine removed from the perfusate. Using 10(-4) M propranolol, a saturation process became evident, whereas no concentration dependency was observed for chlorpromazine uptake. Kinetic analysis revealed similar uptake rates, but different capacities for both compounds. In displacement experiments, 10(-9) M propranolol was displaced by 10(-4) M amphiphilic drugs in the order: chlorpromazine greater than propranolol greater than alprenolol greater than tetracaine. No displacement occurred by practolol, indomethacin or phenylbutazone. The results indicate that the lungs have a large binding capacity for amphiphilic drugs. These compounds can interfere with each other, according to their lipophilicity, their steric configuration and charges.

Animals↗
PubMed1988

Evidence for interaction between central beta-2 adrenoceptors and epinephrine pathways in the opioid-induced prolactin rise in the rat.

1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-induced prolactin (PRL) rise was investigated. 2. FK 33824, a synthetic opioid peptide injected into the third ventricle of Wistar male rats, generated a PRL rise that was significantly reduced by pretreatment with IPS 339, a potent and selective beta-2 antagonist. 3. Inhibition of central epinephrine synthesis with SKF 64 139, which selectively blocks phenylethanolamine-N-methyltransferase, partially decreased the PRL release induced by FK 33824. 4. Practolol, a selective beta-1 adrenoceptor blocker, did not modify the PRL secretion induced by FK 33824. 5. The results indicate that this FK 33824-induced PRL rise depends in part on the functional integrity of central beta-2 adrenoceptors and that epinephrine pathways in the brain may play an important role in the mechanisms by which opioid peptides increase PRL secretion.

Animals↗
PubMed1986

Inhibition of quinidine-propranolol elevation of the ventricular fibrillation threshold by bilateral stellectomy+vagotomy in the anesthetized dog.

The antiarrhythmic potentiation that occurs with the coadministration of quinidine-propranolol has been attributed to propranolol-induced cardiac beta adrenergic receptor blockade. That this may not be the sole mechanism, however, is suggested by the finding that sotalol, pronethalol and practolol fail to potentiate quinidine in some antiarrhythmic tests. Thus, in the present experiments, the influence of bilateral stellectomy + vagotomy on quinidine-propranolol antiarrhythmic activity was studied in the anesthetized dog. Antiarrhythmic activity was determined as elevation of the electrical ventricular fibrillation threshold (VFT) when the left ventricle was stimulated directly with 60 Hz, 6 msec and varying mA for 2 sec. The increase in VFT produced by quinidine-propranolol (5 + 0.2 mg/kg, i.v.) was significantly reduced when the heart was subsequently denervated by bilateral stellectomy + vagotomy. The cardiac denervation did not significantly reduce the elevation of VFT that had been produced by prior administration of propranolol 0.4 mg/kg or sotalol. In other groups with prior bilateral stellectomy + vagotomy, the separate administration of propranolol 0.4 mg/kg or quinidine 5 mg/kg failed to significantly elevate the VFT although the VFT was increased by propranolol 0.8 mg/kg. The results indicate that the action of quinidine-propranolol to elevate the VFT may be dependent in part upon an intact nerve supply to the heart.

Anesthesia↗
PubMed1979

[Long-term studies on the beta blocker talinolol (cordanum) with special reference to side effects].

224 patients with coronary heart disease, hypertension, disturbances of cardiac rhythm or hyperkinetic heart syndrome were treated with the cardioselective beta-blocker Talinolol (Cordanum) for a period up to 3 years. In 239 examinations in intravenous or peroral application of this medicament we controlled among others the appearance of side effects. This test was carried out with the help of standardised questionings and clinical controls. Apart from registrations of ECG and blood pressure clinico-chemical investigations were included and in the long-term experiment also tests by dermatologists, otorhinolaryngologists and ophthalmologists. In the total number of patients the proportion of side appearances was 17,6%, in the long-term experiment (100 patients with on an average 12.9 months) 7%. The symptoms most frequently cited in the initial phase, such as fatigue, weakness, insomnia and nausea receded within 4 weeks apart from few exceptions. There did not appear any essential bradycardic disturbances of the cardiac rhythm, just as little were references to disadvantageous reactions in the sense of a practolol syndrome.

Adolescent↗
PubMed1979

Antihypertensive effects of intra-cisternal beta-blocking agents in dogs with acute nerogenic hypertension.

Dl-propranolol, acebutolol, atenolol, bupranolol, oxprenolol, pindolol, practolol, sotalol and d-propranolol were injected into the cisterna magna of anesthetized dogs with neurogenic hypertension induced by deafferentation and vagotomy. Dl-propranolol and bupranolol correct the hypertension and the tachycardia of the debuffered dog, whereas oxprenolol has only an action on the heart rate. The other beta-blocking drugs and d-propranolol were inactive at the doses used. Our results show that a mere central effect cannot explain the antihypertensive properties of all the tested beta-blocking agents.

Adrenergic beta-Antagonists↗
PubMed1979

[Effect of beta-adrenergic drugs on humoral immune response factors].

The authors examined the influence of beta-adrenergic stimulators Isoprenaline and Salbutamol as well as beta-adrenergic blockers Propranolol, Practolol and Pindolol on the proliferation of cells, forming plaques, 7S-immunoglobulins, hemagglutination titres and hemolytic activity of the complement. Primary stimulation with subsequent inhibition was induced by beta-adrenergic agonists and inhibition--by beta blocker Propronanol in a base of 10 mg/kg on the proliferation of cells, forming antibodies. The results were in correlation with hemagglutination titres. Salbutamol and beta-blockers inhibited immune hemolysis. The mechanisms of the observed effect are discussed in respect to the specific and nonspecific effect of the drugs used.

Adrenergic beta-Agonists↗
PubMed1979

[Betablockers and skin (author's transl)].

Up to now betablockers, with the exception of erythermalgia, have been rarely used as therapeutic agents in dermatology. However, cutaneous drug reactions are numerous. A review of the literature about practolol cutaneous effects and their possible mechanisms has shown that a great variety of clinical states can be encountered. All betablockers have been known to produce harmful side effects, although less frequently. In conclusion, the description of each new case of cutaneous drug reaction probably due to betablocker must be assessed.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Role of the autonomic nervous system in early arrhythmias in acute myocardial infarct in the rabbit].

In order to evaluate the influence of the autonomic nervous system in the incidence and characteristics of the early arrhytmias that follows myocardial infarction, we have developed an experimental myocardial infarction in rabbits by acute occlusion of the left ventricular artery. The influence of adrenergic and cholinergic suppression over rhythm disorders and hemodynamics changes after experimental infarction in the rabbit was also studied. We found that after the acute experimental infarction in the rabbit heart, arose an early stage of rhythm disorders in 60% of the animals. In a group of animals that were injected with Practolol before coronary occlusion, the incidence of arrhythmias was 25% and in a group of animals with vagotomy prior to occlussion none of them developed rhythm disorders. It was concluded that the model is highly steemed for the study of early arrhytmias and that automatic nervous system has an important role in the incidence of such arrhythmias.

Acute Disease↗
PubMedDate not supplied

Possible mechanism of hydrocortisone induced eosinopoenia.

Hydrocortisone (HC) injection in rabbits induced eosinopoenia (reduction in absolute eosinophil count) which could be successfully abolished by beta--adrenoceptor antagonists, a propranolol, sotalol, practolol and H 35/25 but not by alpha--adrenoceptor antagonist, phenoxybenzamine. Reserpine per se produced eosinopoenia followed by eosinophilia. However, reserpine pretreatment failed to abolish HC-induced eosinopoenia. It is suggested that the eosinopoenia is mediated through beta--adrenoceptors, which could not be differentiated into beta 1/beta 2--adrenoceptor subtypes as has been possible for other beta-adrenoceptor mediated responses.

Animals↗