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PubMedDate not supplied

Beta 1-selectivity of bisoprolol, a new beta-adrenoceptor antagonist, in anesthetized dogs and guinea pigs.

The beta-adrenoceptor activity of the newly synthesized antagonist bisoprolol [+/-)-1-[4-(2-isopropoxyethoxymethyl)-phenoxy]-3-isopropylamino-2- propranol, hemifumarate), has been compared with the effect of several reference compounds in anesthetized dogs and guinea pigs. In anesthetized, bivagotomized dogs, isoprenaline dose-response relations for increase in heart rate and decrease in diastolic blood pressure were established. Bisoprolol had the largest beta 1/beta 2 ratio, i.e., 147 (102-292). Practolol showed a beta 1/beta 2 ratio greater than 17; betaxolol 6-15; acebutolol, atenolol, and metoprolol 1.1-3.2; mepindolol 0.6-1 and propranolol 0.2. In artificially ventilated guinea pigs, the activity of bisoprolol on histamine-induced increase in tracheal lateral pressure (TLP) and basal heart rate (HR) was tested: using doses taken at TLP (30 mm Hg) and HR (250 beats/min), bisoprolol exhibited the most pronounced ratio TLP/HR of 124 +/- 59, followed by atenolol 33 +/- 23, metoprolol 25 +/- 15, betaxolol 12 +/- 4, propranolol 1 +/- 0.3, and celiprolol 0.23 +/- 0.19. These experiments indicate that bisoprolol possesses a pronounced beta 1-selectivity, which seems to be superior to that of known beta 1-selective antagonists.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Beta-adrenoceptor subtypes in human, rat, guinea pig, and rabbit atria.

Selective beta-adrenoceptor agonists and antagonists were used to characterize the beta-adrenoceptor subtypes in human right atrium. The activity order of selective agonists for rat, guinea pig, and rabbit atrial inotropic and chronotropic responses was consistent with the hypothesis that only beta 1-adrenoceptors mediate these responses. In human right atrium, however, the beta 2-selective agonists fenoterol and salbutamol were relatively much more active. The beta 1-selective antagonist practolol preferentially antagonized the human atrial response to noradrenaline (beta 1-selective) as opposed to fenoterol (beta 2-selective), whereas the beta 2-selective antagonist ICI 118,551 preferentially antagonized the response to fenoterol. The data indicate that the response of human right atrium to beta-adrenoceptor agonists is mediated by a mixed beta 1-plus beta 2-adrenoceptor population. The implications of these results with respect to the therapeutic uses of beta-adrenoceptor agonists are discussed.

Adrenergic beta-Agonists↗
PubMed1980

Antiarrhythmic effects of four different beta-adrenergic blockers in the mouse chloroform arrhythmia model.

The antiarrhythmic activity of four different beta-adrenergic blockers was assessed in the mouse chloroform arrhythmia model. ED50 values and 95% confidence intervals established by i.p. administration of drug were: propranolol (22.8, 10.9--67.0 mg/kg), sotalol (38.0, 15.9--58.5 mg/kg) and practolol (167, 111--235 mg/kg). Butoxamine provided some protection against the arrhythmia within a narrow dose range (53 to 79 mg/kg).

Adrenergic beta-Antagonists↗
PubMed1980

Altered pharmacokinetics of beta-adrenoceptor blocking drugs in patients with renal insufficiency.

Altered pharmacokinetics of beta-adrenoceptor blocking drugs in renal insufficiency are described in the light of available data in the literature and current knowledge based on recent investigations with a variety of commonly used drugs. Reduced excretion and retention of the active drug is not the only abnormality that may occur in renal insufficiency. Alterations in drug absorption, protein binding, volume of distribution, biotransformation and accumulation of pharmacologically active metabolite are important factors to consider--all may play an important role in determining altered pharmacologic or toxicologic response to a drug. Our own observations on altered disposition kinetics of the three beta-adrenoceptor blocking drugs practolol, sotalol and acebutolol in patients with renal insufficiency are also included in this paper.

Adrenergic beta-Antagonists↗
PubMed1980

[Beta blockers and disturbances of the microcirculation (author's transl)].

Study of 192 cases of hypertensive patients, 89 of whom were treated by diet, general advice and correction of risk factors for an average period of 8 months. The group of patients treated beta blockers consisted of 103 subjects, 28 of whom received Propranolol, 29 Oxyprenolol, 20 Atenolol and 26 Practolol. The prevalence of Raynaud's phenomenon was markedly greater in the patients treated with beta blockers, in comparison with the group not receiving any drugs. The highest incidence of vasomotor problems was seen in the group of subjects treated with Propranolol, with 57% of patients having a Raynaud-type paroxysmal acrosyndrome. In more than half of the cases attributed to Propranolol, the clinical picture of Raynaud's syndrome was severe. Discussion of the mode of action of beta blockers on the microcirculation.

Adrenergic beta-Antagonists↗
PubMed1980

[The effect of atenolol on the cardiovascular system (author's transl)].

Effects of atenolol on the cardiovascular system were studied in rats and dogs. Atenolol (10 microgram/kg - 3 mg/kg) did not increase heart rate significantly in rats pretreated with reserpine (5 mg/kg), while a significant increase occurred with practolol (30 microgram/kg - 3 mg/kg). Atenolol (100 microgram/kg) inhibited the response of canine heart (heart rate and myocardial contractile force) to isoproterenol to a similar degree as seen with propranolol (100 microgram/kg) did. The ability of atenolol to inhibit vasodilating action of isoproterenol, however, was about 1/12 of that of propranolol. Atenolol (0.5 mg/kg) did not inhibit hemodynamic responses to ouabain and CaCl2 in dogs, while this drug inhibited these responses to isoproterenol. Atenolol decreased heart rate, myocardial contractile force, left ventricular pressure, and rate of rise of the left ventricular pressure (dp/dt LV max) dose-dependently. Atenolol (1 mg/kg) decreased coronary venous outflow and myocardial oxygen consumption in dogs, but did not alter the myocardium to a more reduced state, as determined by coronary arterial and venous lactate and pyruvate levels. These results confirmed that atenolol is a potent cardioselective beta-blocker devoid of intrinsic sympathomimetic action. The results also suggest that atenolol inhibits cardiac function without disturbing the intracellular redox state of the myocardium.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Comparative effects of seven beta adrenolytic agents on blood pressure after injection into the posterior hypothalamus of rats. The frequency heart and the plasma renin activity (author's transl)].

The author's studied the central action of seven beta-blocking agents: alprenolol, atenolol, bupranolol, oxprenolol, pindolol, practolol, propranolol. The drugs were stereotactically injected into the posterior hypothalamus of non anaesthesized rats. Three dosages were used. Blood pressure, heart rate and plasma renin activity (PRA) were recorded. 2. The seven beta-blocking drugs used decreased heart frequency for at least one dosages PRA always decreased but blood pressure was lowered only after administration of alprenolol, oxprenolol, pindolol. 3. The discussion deals with: --the specificity of the target, --the involvement of the central beta receptors into the PRA regulation, --the correlations between the cardiovascular responses and the pharmacological properties of the different molecules; the hypothetic role of the intrinsic activity is postulated --the dissociation between heart rate and blood pressure responses, suggesting the existence of two different receptors for the specific control of those two parameters.

Adrenergic beta-Antagonists↗
PubMed1981

[Effect of beta adrenergic receptor agonists and blockaders on the action of bradykinin].

A study was made of the effect of beta-adrenomimetics (isoprenaline, orciprenaline, inoline) and beta-adrenoblockers (propranolol, pindolol, oxprenolol, atenolol and practolol) on changes in the tone of smooth muscles of an isolate ileum of guinea-pigs, increase in microvascular permeability and depressor reaction in rats induced by bradykinin. beta-Adrenomimetics decreased spasmogenic and microcirculatory effects of bradykinin. Depending on the selectivity and presence of partial agonistic activity, beta-adrenoblockers exerted different influence on changes in the tone of extravasal muscles and permeability induced by bradykinin. In doses of 0.1, 0.5 and 1 mg/kg (intravenously) beta-adrenoblockers potentiated and prolonged the depressor effect of bradykinin.

Adrenergic beta-Agonists↗
PubMed1982

[Studies on the blood pressure of beta-adrenoceptor blocking drugs, particularly in relation to the mechanism of the pressor action induced by beta-adrenoceptor blocking drugs in rats (author's transl)].

Several investigators have confirmed that beta-adrenoceptor blocking drugs produced a sustained pressor action in anesthetized rats. However, the mechanism of the pressor action has not been sufficiently explored. The following studies were done to further investigate the mechanism. (a) effects of pindolol, carteolol, propranolol, alprenolol, practolol and acebutolol (0.015-0.3 mumole/kg i.v.) on blood pressure of anesthetised rats, b) effects of these drugs on the positive chronotropic action and vasodilation induced by isoprenaline (0.1 microgram/kg i.v.) in anesthetized rats, c) effects of these drugs on the increase in heart rate and contractile force of isolated rat and guinea pig atria induced by isoprenaline, d) effects of these drugs on the relaxation of isolated guinea pig trachea induced by isoprenaline. From these experiments, the magnitude of the pressor action of beta-adrenoceptor blocking drugs in anesthetized rats was found to be more closely related to the magnitudes of inhibition produced by beta-adrenoceptor blocking drugs on isoprenaline-induced relaxation of isolated guinea pig trachea and on isoprenaline-induced vasodilation in anesthetized rats than to those on isoprenaline-induced positive chronotropic and inotropic actions of isolated atria.

Adrenergic beta-Antagonists↗
PubMed1982

[Pharmacological basis for the therapy of cardiovascular disease with beta-adrenoceptor blocking drugs (author's transl)].

The introduction of beta-adrenoceptor blocking drugs initiated a breakthrough in the treatment of various cardiovascular disorders within the last 20 years. The major cardiac indications for beta-blockers are coronary heart disease, hypertension and arrhythmias. No one beta-adrenoceptor blocking drug has been shown to be more efficacious than another, and efficacy can be related to the stereo-selective blockade of adrenergic beta-receptors. The major side effects and the contraindications are mainly due to beta-adrenoceptor blockade in combination with the organ-specific distribution of beta 1- and beta 2-adrenoceptors. In addition to their specific antagonism beta-receptor blocking drugs can differ in beta 1-adrenoceptor selectivity, intrinsic sympathomimetic activity (ISA) as well as in nonspecific effects. However, these ancillary properties do not seem to be of importance for the therapeutic effect of these drugs. A relative beta 1-selectivity is probably able to reduce the incidence of side effects e.g. in asthmatics, in diabetic patients and in patients with peripheral vascular disease, however, beta-adrenoceptor antagonists should be used with caution in these patients, At the present time, there is no convincing evidence that beta-adrenoceptor antagonists with partial agonist activity are superior in patients with congestive heart failure or in asthmatics. Except at high dosages the nonspecific local anaesthetic or cardiodepressant effects of lipophilic beta-adrenoceptor antagonists (propranolol-oxprenolol-group) also do not seem to be of importance in the therapy of cardiovascular diseases. On the other hand, lipophilicity of a lipophilic beta-adrenoceptor antagonists of the propranolol-oxprenolol-group exhibit serum half-lives in the range of two to six hours, whereas half-lives of six to 24 hours are found with the hydrophilic compounds sotalol, practolol, nadolol and atenolol, respectively, while with regard to lipophilicity and serum half-lives timolol, metoprolol, pindolol and acebutolol fall midway between these extremes. It was well established that the duration of action of the beta-adrenoceptor antagonists is about two or three times longer than would be expected from the pharmacokinetic data. This can be explained by the fact that the pharmacodynamic effect obeys zero order kinetics whereas the decline in serum concentration follows first order kinetics. The pharmacokinetic and pharmacodynamic data of the beta-adrenoceptor blocking drugs are of great value in the therapy inasmuch as the dosage interval must be modified accordingly: whereas the lipophilic compounds have to be taken two to four times per day, one dosage per day seems sufficient with the hydrophilic compounds.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of beta-receptor antagonists on HgCl2-induced acute renal failure in rats.

During the first 48 h of HgCl2-induced acute renal failure (ARF), a single intraperitoneal injection of 100-100 micrograms/kg of the beta-adrenergic blockers pindolol, propranolol and practolol caused a significant rise in urinary sodium excretion and a decrease in plasma renin activity (PRA), renal cortical renin activity (RRA) and urinary catecholamine excretion. A single intraperitoneal injection of 3 mg/kg HgCl2 resulted in ARF characterized by progressive azotemia, a transient increase in PRA, a progressive rise in RRA and urinary catecholamine excretion. After pretreatment with these beta blockers, PRA, RRA and urinary catecholamine excretion remained unchanged and azotemia was markedly reduced; urine flow rates did not fall, and were significantly higher than control flows till after 48 h. These results indicate that pretreatment with beta blockers decreases the severity of ARF, though they cannot prevent is; that increased activity of the sympathetic nervous system is involved in ARF and that increase in RRA may be an aggravating factor in the pathomechanism of the nephrotoxic model in ARF.

Acute Kidney Injury↗
PubMed1982

[Effect of talinolol on the activity of the mixed-function oxidases of rat liver].

Experiments with male rats were performed to compare the in vitro and in vivo effects of talinolol with those of propranolol, alprenolol, practolol, proadifen (SKF 525-A) and barbital. Three in vitro model reactions (amino-phenazone N-demethylation, p-nitroanisol O-demethylation and aniline hydroxylation) as well as the hexobarbital lateral-position time served as parameters. The results obtained show that talinolol, like the other beta-receptor blockers, can inhibit polyfunctional oxidases. There were no indications of an inductive action.

Adrenergic beta-Antagonists↗
PubMed1983

Secondary prevention of myocardial infarction with drugs.

Clinical trials in the field of secondary prevention of myocardial infarctions are reviewed, with emphasis on those studies that were randomized and included at least 100 patients. Standardized total mortality data, when available, are provided. Five groups of drugs are reviewed: 1) antiarrhythmic drugs, including studies of phenytoin, tocainide, mexiletine and aprindine. Important, commonly used drugs in this group, which apparently have not been submitted to clinical trials, include procainamide and lidocaine; 2) lipid-lowering drugs, including estradiol, conjugated equine estrogen, dextrothyroxine, clofibrate and nicotinic acid; 3) anticoagulant drugs, the oldest and most controversial preventive drug measure. In this group, only the oral drug derivatives of indandione or coumarin have been tested, and no appropriate studies of parenteral heparin were found; 4) platelet-active drugs--six studies dealing with aspirin alone, one combining aspirin and dipyridamole, and one study of sulfinpyrazone are reviewed; and 5) beta-adrenergic blocking drugs, including practolol and timolol.

Adrenergic beta-Antagonists↗
PubMed1983

The human heart beta-adrenergic receptors. I. Heterogeneity of the binding sites: presence of 50% beta 1- and 50% beta 2-adrenergic receptors.

Beta-adrenergic receptors were characterized in a particulate fraction of human auricles obtained from patients operated upon for coronary insufficiency or valvular disease. [125I] Hydroxybenzylpindolol binding was evaluated in terms of kinetics; KD and Bmax values; and inhibition of binding in the presence of 10 microM GTP and of increasing concentrations of four nonselective agonists giving a Hill coefficient of 1 (isoproterenol, salbutamol, fenoterol, and epinephrine), of two nonselective antagonists giving a Hill coefficient of 1 (pindolol and propranolol), and of a series of selective drugs giving a Hill coefficient of 0.60-0.72 that included three beta 1-selective antagonists (practolol, metoprolol, and atenolol) and two beta 2- selective agonists (procaterol and zinterol). KD values for all drugs were compatible with the coexistence in membranes from human auricles of beta 1- and beta 2-adrenergic receptors, the relative proportions of receptors of each subclass being approximately the same.

Adrenergic beta-Agonists↗
PubMed1983

The human heart beta-adrenergic receptors. II. Coupling of beta 2-adrenergic receptors with the adenylate cyclase system.

The beta-adrenergic stimulation of adenylate cyclase in membranes from human auricles, ventricles, and fetal heart was compared with the binding properties of beta-adrenergic receptors in human auricles. In terms of adenylate cyclase activation, three full agonists (isoproterenol, epinephrine, and norepinephrine), four partial agonists (procaterol, salbutamol, fenoterol, and zinterol), and four antagonists (propranolol, metoprolol, atenolol, and practolol) were tested. The beta-adrenergic activation of adenylate cyclase in membranes from rat heart (with a majority of beta 1-adrenergic receptors), rat erythrocytes, and rat reticulocytes (with a homogeneous population of beta 2-adrenergic receptors) served as reference. The reactivity of human heart adenylate cyclase, estimated by the Kact or Ki values of 11 beta-adrenergic agents, indicated that the activation of this enzyme occurred through receptors of the beta 2-subtype only. Receptors of the beta 1-subtype (50% of the total population) were not coupled to the enzyme.

Adenylyl Cyclases↗
PubMed1983

Desensitization of beta adrenergic receptors linked to adrenocorticotropin secretion.

Stimulation of beta adrenergic receptors on AtT-20 cells increases intracellular cyclic AMP levels and adrenocorticotropin hormone (ACTH) release. Pretreatment of these cells with catecholamines reduces the ability of (-)-isoproterenol to stimulate both cyclic AMP formation and ACTH secretion. This beta receptor desensitization is time- and dose-dependent and is reversible. Various beta adrenergic agonists can induce this desensitization with a rank order of potency of salmefamol greater than or equal to (-)-isoproterenol greater than or equal to epinephrine greater than or equal to norepinephrine greater than or equal to (+)-isoproterenol. (+/-)-Propranolol but not practolol can block the (-)-isoproterenol-induced beta receptor desensitization. Long-term treatment of AtT-20 cells with (-)-isoproterenol reduces the density of beta receptors but does not affect the affinity of these sites for [3H]dihydroalprenolol. In addition to desensitizing beta receptors, (-)-isoproterenol pretreatment enhances basal ACTH secretion. This effect was dose-dependent and blocked by (+/-)-propranolol. Forskolin-stimulated cyclic AMP formation and ACTH secretion was not altered by (-)-isoproterenol treatment indicating that the desensitization of beta receptors on AtT-20 cells is the result of receptor-adenylate cyclase uncoupling. No cross-desensitization of corticotropin releasing factor or vasoactive intestinal peptide receptors occurred as (-)-isoproterenol treatment did not alter the effect of these peptides on cyclic AMP synthesis or ACTH secretion.

Adrenergic beta-Agonists↗
PubMed1983

Pharmacology of 4-(2-hydroxy-3-[(1-methyl-3-phenylpropyl)-amino]propoxy)benzeneacetamide (KF-4317).

4-(2-Hydroxy-3-[(1-methyl-3-phenylpropyl)amino] propoxy)benzeneacetamide (KF-4317) differs from conventional adrenoceptor antagonists in producing a competitive blockade at both alpha- and beta 1-adrenoceptors. In blocking beta 1-adrenoceptors, KF-4317 is as active as labetalol in both in vitro and in vivo experiments, and 22 times less potent (in vitro) and 2 times less potent (in vivo) than propranolol. In blocking beta 2-adrenoceptors, KF-4317 is 776 times less potent (in vitro) and 83 times less potent (in vivo) than propranolol. The ratio of beta 1-blocking activity to beta 2-blocking activity is 33 to 145 for practolol, 37 for KF-4317, 1 for propranolol and 0.16 to 1 for labetalol, respectively. In blocking alpha-adrenoceptors, KF-4317 is 55 times less potent than phentolamine and 6 times less potent than labetalol in in vitro experiments, but as active as labetalol in in vivo experiments. These results show that KF-4317 possesses a novel type of adrenoceptor antagonistic property.

Adrenergic alpha-Antagonists↗
PubMed1983

[Antinuclear antibodies and lupus induced during treatment of arterial hypertension. Role of beta-blockers and alpha-methyldopa].

Comparison of hypertensive patients receiving no treatment with subjects of the same age reveals the presence of antinuclear antibodies in twice as many of the former as the latter. Various antihypertensive drugs increase this prevalence. They may induce iatrogenic lupus. Alpha-methyldopa: the frequency of antinuclear bodies is three times greater than in untreated hypertensive patients. However there are no reported cases of clinical symptomatology of induced lupus. Beta-blockers. Practolol, acebutolol, labetalol, atenolol, timolol, metoprolol, pindolol and oxprenolol are suspected of increasing antinuclear antibodies. These drugs may be weak inducers of iatrogenic lupus when compared with major drugs: procainamide, high doses of hydralazine and D-penicillamine.

Adrenergic beta-Antagonists↗