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At least 829 records · Page 46Linked to original sources
PubMed1980

Hemodynamic reactions under various stimuli before and during chronic beta-blockade.

Chronic beta-blockade with the cardioselective blockers practolol and atenolol had no attenuating effect on blood-pressure increases provoked by cold pressor test or by plasma expansion. Reports in the literature of an exaggerated cold pressor test reaction under propanolol therapy could be confirmed with practolol and atenolol. This may be regarded as an advantage of cardioselective blockade. The increase of the cardiac output after plasma expansion is enhanced during cardioselective beta-blockade. This could result from a reduced action of cardioselective blockers on the capacitance vessels. Concerning the mechanisms of antihypertensive action of beta blocking agents our findings do not support the cardiac output hypothesis. Before and during beta blocking therapy baroreflex sensitivy was not significantly different. So the baroreflex theory can't be strengthened neither.

Adrenergic beta-Antagonists↗
PubMed1980

[Effect of adrenergic beta-receptor blockers on the oxygen consumption or narcotized rats and the calorigenic action of adrenaline].

The adrenergic beta-receptor blockers: Propranolol, Alprenolol, Oxprenolol, Pindolol, Practolol, and Talinolol, inhibit the calorigenic action of adrenaline in experiments on rats. These findings doe not permit any quantitative comparison, because the beta blockers show considerable differences in their inherent action on the basic metabolism. THe cardioselective beta-blockers, Practolol and Talinolol, are without effect, while Propanolol increases, and Alprenolol, Oxprenolol and Pindolol lower the basic metabolism. The intrinsic activity of these compounds increases with the decrease of their hydrophobicity.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of different beta-blocking agents on an in vitro model of ventricular automaticity.

The effect of 7 beta-blocking agents with different properties such as quinidine like activity (QLA) or intrinsic sympathomimetic activity (ISA) was tested on a model of automaticity induced in the isolated right ventricle of the rat. The following results were obtained: a) Propranolol was the most effective drug for the inhibition of the automatic activity; b) Pronethalol, pindolol and labetalol also decreased the automatic rate. Acebutolol was less effective than these three drugs but with larger concentrations also decreased the preparation's frequency; c) Neither sotalol nor practolol decreased the preparation's frequency, but practolol increased that frequency at higher concentrations. We conclude that QLA might play an important role in the antidysrhythmic efficacy of these compounds which might be antagonized by ISA.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Effect of some beta-adrenoceptor blockers and of (+) propranolol on adrenaline-induced pulmonary edema in mice.

(+) Propranolol is considered to prevent adrenaline-induced pulmonary edema (A.P.E.) due to the beta-adrenoceptor blockade. However, local anaesthetics also are known to prevent pulmonary edema. To assess the role of beta-adrenergic blockade in A.P.E., the effect of a beta 1-blocker possessing local anaesthetic action (+/- Metaprolol) and a beta 1-blocker possessing no local anaesthetic action (+/- practolol) was studied along with propranolol derivatives. The study revealed that (+), (-), (+/-) propranolol and (+/-) metaprolol completely prevented A.P.E. whereas (+/-) practolol did not. This shows that local anaesthetic action but not the-beta adrenergic blockade may be responsible for prevention of A.P.E.

Adrenergic beta-Antagonists↗
PubMed1983

Activation of beta 2-adrenergic receptors on mouse anterior pituitary tumor cells increases cyclic adenosine 3':5'-monophosphate synthesis and adrenocorticotropin release.

AtT-20 cells comprise a mouse anterior pituitary tumor cell line that synthesizes and secretes adrenocorticotropin hormone (ACTH). beta-Adrenergic receptors were characterized on AtT-20 cells using receptor binding methodology and the ability of beta-receptor agonists to stimulate intracellular cyclic adenosine 3':5'-monophosphate (cAMP) formation and the release of ACTH immunoreactivity. The density of beta-receptors on membrane preparations of these cells is 64 fmol/mg of protein and their affinity constant (KD value) for tritiated dihydroalprenolol is 11 nM. The binding of [3H] dihydroalprenolol to AtT-20 cells is stereoselectively inhibited by propranolol and isoproterenol but is not affected by phentolamine. The beta-receptors on these cells appear to be of the beta 2-receptor subtype since a selective beta 2-receptor agonist, salmefamol, can inhibit [3H]dihydroalprenolol binding, whereas practolol, a beta 1-receptor blocker, is ineffective. (-)-Isoproterenol stimulates cAMP formation in AtT-20 cells and this effect is blocked by dl-propranolol. Both l-epinephrine and l-norepinephrine induce dose-dependent increases in cAMP formation with the former agonist being more potent. Salmefamol also stimulates cAMP formation in these cells. The secretion of ACTH from AtT-20 cells is induced by (-)-isoproterenol as well as by other adrenergic agonists. The isoproterenol effect on ACTH release is stereoselective, calcium dependent, and blocked by dl-propranolol but not by phentolamine or practolol.

Adrenocorticotropic Hormone↗
PubMed1982

Inhibitory mechanism of methamphetamine in the isolated myocardium of bullfrog.

In the isolated heart of the bullfrog, both the spontaneous contractile force of the atrium and the electrically-induced contractile force of the ventricle were enhanced by the initial administration of methamphetamine. However, a second administration of the drug caused a dose-dependent negative inotropic effect. The methamphetamine-induced positive inotropic effect was reduced or abolished by either practolol or cocaine pre-treatment. The negative inotropic effect of methamphetamine was markedly attenuated after theophylline or practolol pre-treatment, but was not affected by cocaine, atropine and phentolamine pre-treatment. Methamphetamine caused a slight decrease of the adenylatecyclase activity of the intact myocardium. It also inhibited not only the cardiac excitation (contractile force and rate) but also the facilitation of adenylatecyclase activity induced by isoproterenol. A slight reduction of the methamphetamine-induced ventricular inhibition was observed by increasing the external calcium concentration; however, the inhibition was not affected by MnCl2 or verapamil pre-treatment. From these results, it is suggested that the inhibitory effect of methamphetamine on the heart may be produced through the blocking of post-synaptic beta-adrenoceptors.

Action Potentials↗
PubMedDate not supplied

[Effect of anesthetics on the cardiac chronotropic reactions induced by isoproterenol].

Some anesthetics were shown to diminish the intensity of positive chronotropic reactions of the cat heart induced by isoproterenol. As measured by the effect exerted, the anesthetics tested can be ranged as follows: a mixture of urethane and alpha-chloralose > nembutal > hexenal > urethane, alpha-chloralose, ether. Ftorotan does not affect the intensity of these reactions. By the effect intensity urethane, alpha-chloralose, ether, hexenal and nembutal correspond with that of practolol in a dose of 15 mg/kg, while the mixture or urethane and alpha-chloralose with that of practolol in a dose of 30 mg/kg.

Anesthetics↗
PubMed1976

Electrocardiographic surface mapping of the heart following myocardial infarction and the influence of beta-blockade.

It is generally accepted that ST segment elevation is one of the characteristic electrocardiographic features of acute myocardial infarction. In experimental myocardial infarction the degree of ST segment elevation has been related to the degree of change in coronary flow. Surface mapping in patients of the electrocardiographic potentials gives an indirect representation of the epicardial ST segment change and in indication of the area of underlying myocardial damage. A number of patients who had sustained myocardial infar-tion within 72 hours were studied. All the patients had a history of prolonged ischaemic cardiac pain, electrocardiographic changes and a rise in serum enzymes. Electrocardiagrams were recorded from 72 points on the chest surface. Control maps were constructed from the ST segment changes measured at each of these points and plotted on a standard diagram. Electrocardiograms were recorded during a control period immediately before 20 mg of practolol was given intravenously over a period of five minutes. In all patients practolol produced a significant reduction in the area of ST segment elevation as represented by a reduction in the number of points with ST elevation of more than 2 mm. The significance of these findings is discussed.

Heart Rate↗
PubMed1999

Quantitative determination of clenbuterol enantiomers in human plasma by high-performance liquid chromatography using the macrocyclic antibiotic chiral stationary phase teicoplanin.

We report a method for the high-performance liquid chromatographic (HPLC) chiral separation of racemic clenbuterol in human plasma. Human plasma was spiked with stock solutions of clenbuterol hydrochloride and practolol as the internal standard. Following a liquid-liquid extraction procedure with 10% (+/-)-2-butanol/isopropyl ether under alkaline conditions, the dried samples were reconstituted in methanol and chromatographed using a macrocyclic antibiotic chiral stationary phase (CSP) known as Chirobiotic T(trade mark) (teicoplanin). The mobile phase composition was methanol:acetonitrile (70:30, v/v), containing 0.3% (v/v) acetic acid and 0.2% (v/v) triethylamine. The resulting chromatogram achieved baseline separation for the clenbuterol enantiomers. Calibration curves (peak area ratio vs plasma concentration, n = 10) were constructed for the (-)-R-and (+)-S-clenbuterol enantiomers with a plasma concentration range of 0. 25-10 microM. The correlation coefficient (r) range was 0.99988-0. 99999 (mean = 0.99999). The lowest concentration measured was 0.25 microM. Inter- and intra-assay variation was determined for the lowest, medium and highest plasma concentration (0.25, 2 and 10 microM) by calculating the analytical recoveries with a range of 96-104%. The percentage recoveries for the clenbuterol enantiomers were 88.4-102% over the concentration range used. Detailed methodology is presented.

Chromatography, High Pressure Liquid↗
PubMed1977

Evidence that catecholamines are not the afferent transmitter in the cochlea.

Beta-receptor blocking agents (practolol, propranolol) and alpha-receptor blocking agents (phenoxybenzamine, phentolamine), when applied intracochlearly do not eliminate the afferetn discharges or compound action potential of the cochlear nerve. Under the assumption that the drugs used reach the synaptic site, it is therefore concluded that these drugs do not interfere with afferent synaptic transmission. Phentolamine,, however, has a toxic effect upon the cochlea independent from the synaptic process. Local application of catecholamines does not increase spontaneous activity of single fibres of the cochlear nerve. These findings show that catecholamines are not likely to be the afferent transmitter.

Acoustic Stimulation↗
PubMed1979

Comparison of the effects of nine beta-adrenergic blocking agents on intraocular pressure in rabbits.

The intraocular pressure lowering effects of nine beta-adrenergic receptor blocking agents were compared using two different models of experimental ocular hypertension in rabbits. All the nine drugs possess, to different extents, a clear pressure-lowering action after topical administration into the conjunctival sac. For potency and duration of action, the best results were obtained with timolol and sotalol. Pindolol, oxprenolol, practolol, and propranolol are also fairly potent while less impressive effects were produced by atenolol, butidrine, and metoprolol. With the exception of propranolol, all the drugs were well tolerated by the ocular tissues.

Adrenergic beta-Antagonists↗
PubMed1976

Effects of beta blockade and atropinisation on plasma catecholamine concentration during exercise.

The changes in plasma catecholamine concentration (deltaC) following beta-blockade (practolol, 15 mg) and atropinisation (Atropine, 1.8 mg) have been studied on 5 healthy male subjects during exercise on a motor driven treadmill. The results showed that for a given V-2 and % VO2 max, beta blockade was without effect on delta C (except in one athletic subject, but atropine produced a rise in deltaC. In relation to Q, both drugs produced an increase in deltaC, but for a given cardiac frequency (fH) deltaC was higher with beta blockade, and lower with atropinisation than found in control experiments. The intra- and inter-subject variability of delta C in relation of fH was resolved by considering the change in cardiac frequency calculated from baseline value obtained during walking at 6.44 km/h on the level, and expressed as a percentage of the maximal fH attainable for given individuals under the different drug and control conditions (%deltafH). It was concluded that during short term exercise, the rise of deltaC in relation to %deltafH reflects both the myocardial sensitivity to vagal and beta blockade, and the circulatory vasoconstrictor control of blood vessels which is required to sustain increases in systemic and muscle blood flow.

Adult↗
PubMed1975

Effects of adrenergic stimulating and blocking agents on the eccrine sweat secretion in atopic dermatitis and psoriasis.

Quantitative measurements of eccrine sweat secretion following stimulation with adrenaline and terbutaline sulphate, a beta-stimulator, have been performed in patients with atopic dermatitis and psoriasis by means of the electrolytic water analyzer, "Meeco". Seasonal variations were demonstrated, the values being lower in the late autumn. The response to adrenaline could be blocked by phentolamine, an alpha-inhibitor, while propranolol, a beta inhibitor, had no effect.--The response to terbutaline was blocked by atropine and partly by practolol, a beta-inhibitor. Terbutaline induced a larger sweat response than isoprenaline, another beta-stimulator. A beta-receptor mechanism, in some way related to cholinergic receptors, is suggested.

Adrenergic Agonists↗
PubMed1989

Distribution and subtype determination of beta-receptors in the spinal cord of the adult rat.

1. We determined the number of beta-receptors in the whole spinal cord of the adult rat and in the cervical, thoracal, and lumbal/sacral parts. 2. The undivided spinal cord contains 47 +/- 10 fmol/mg beta-receptors (KD = 2066 +/- 982 pmol/liter), and the cervical part of the spinal cord contains 53 +/- 8 fmol/mg protein (KD = 3224 +/- 1775 pmol/liter). The thoracal part shows 40 +/- 1 fmol/mg protein (KD = 3229 +/- 104 pmol/liter), and the lumbal/sacral spinal cord contains 48 +/- 8 fmol/mg protein (KD = 3610 +/- 1610 pmol/liter). 3. Competitive inhibition studies with l-practolol, dl-atenolol, and ICI 118,551 were performed and we calculated by a computer program in the whole spinal cord the following ratio of beta-receptor subtypes: 80 +/- 5% Beta 1-receptors and 20 +/- 5% beta 2-receptors. 4. The basal and (-)-isoproterenol- and NaF-stimulated activity of adenylate cyclase was highest in the cervical part of the spinal cord and equally distributed between the thoracal and the lumbal/sacral parts. 5. The whole synaptosomal protein of the cervical part of the spinal cord contained 132 +/- 20 fmol, the thoracal part 117 +/- 3 fmol, and the lumbal/sacral part 133 +/- 22 fmol.

Adenylyl Cyclases↗
PubMed1978

Direct characterization of beta-adrenoceptors in membranes of immature red blood cells from rats.

By means of the radioactive antagonist ligand (3H)(-) dihydroalprenolol (DHAP) specific binding sites were identified in membrane preparations from red blood cells from rats. These specific sites were characterized as beta-adrenoceptors because of the following reasons: Specific binding of DHAP (in contrast to unspecific binding) was dependent on temperature and time of incubation. Furthermore, specific binding of DHAP showed saturability, temperature-dependent reversibility and high affinity (KD-value of DHAP = 6.51 nM). Specific binding of DHAP was competitively inhibited by beta-adrenergic antagonists (pindolol greater than alprenolol greater than or equal to propranolol greater than practolol) and agonists (isoprenaline greater than adrenaline). The (-) enantiomers of pindolol and isoprenaline showed pronounced higher affinities for the receptor sites than the respective (+) enantiomers. The receptor density in the membrane preparations (pmoles/mg protein) was strongly dependent on the degree of reticulocytosis: The Bmax-values increased more than 4 to 5 fold without alteration of the respective KD-values when reticulocyte counts were enhanced from 3 to 80% treatment of the animals with increasing doses of acetyl phenylhydrazine.

Alprenolol↗
PubMed1977

Side effects and contraindications of beta-receptor blocking agents.

Unwanted effects of beta-receptor blocking agents can be divided into three categories: 1. Those arising specifically from the pharmacologic, i.e., beta-blocking action. 2. Side effects not directly (or not with certainty) related to beta-blockade. 3. Adverse and potentially specific reactions to individual beta-blocking agents. Category 1 covers the majority of adverse effects (heart failure, severe bradycardia and hypotension, arterial insufficiency, increased airways resistance, gastrointestinal symptoms, hypoglycemia). These can largely be avoided by proper selection and preparation of patients. Category 2 covers cutaneous reactions (rashes, alopecia, pruritus), purpura (thrombocytopenic and nonthrombocytopenic) etc. as well as side effects attributable to the central nervous system (antianxiety effects, nightmares etc.). In the third category the "oculo-cutaneous syndrome" associated with practolol is discussed.

Adrenergic beta-Antagonists↗
PubMed1977

The modulation of histamine release by alpha-adrenoceptors: evidences in murine neoplastic mast cells.

Murine neoplastic mast cells which have been loaded with exogenous labelled histamine, released 14C-histamine when exposed to increasing concentrations of phenylephrine and noradrenaline. Adrenaline was only slightly effective, while isoprenaline and dibutyryl-cyclic-AMP were fully inactive. The release of histamine evoked by alpha-adrenergic agonists was antagonized by phentolamine, and left unchanged by practolol and cocaine. It is concluded that alpha-adrenoceptors may be valuable in evoking histamine release by murine neoplastic mast cells.

Animals↗
PubMed1975

Hypercalcemic effect of catecholamines and its prevention by thyrocalcitonin.

Earlier work by others has shown that the catecholamines, epinephrine and isoproterenol, can raise blood calcium levels in parathyroidectomized but not intact rats, and can restrict the hypocalcemic effect of injected thyrocalcitonin (TCT). The present findings support this earlier work, further showing that such catecholamines can produce hypercalcemia in rats after removal of the thyroid gland by acute thyroparathyroidectomy (TPTX) and indicating that these drugs may raise blood calcium by mobilizing calcium from bone. Rats were fasted overnight, subjected to TPTX and concurrently injected with adrenergic agonist or antagonist drugs alone or in combination. Epinephrine, isoproterenol, and the beta-2 adrenergic agonist, salbutamol, in doses greater than or equal to 1 mg/kg raised blood calcium from low normal levels (approximately 9-10 mg/100 ml) by 1.5 to 2 mg/100 ml (p less than 0.01). Hypercalcemia was apparent by 1 hour after injection and lasted for 1-4 hours. The extent of Ca elevation was dose-related. Pretreatment of rats with the alpha-adrenergic antagonist, phenoxybenzamine, enhanced the effect of epinephrine while pretreatment with the beta-antagonist, propranolol, reduced the effect of isoproterenol. The more selective beta-2 antagonist, butoxamine, but not the beta-1 antagonist, practolol, also reduced the hypercalcemic effect of isoproterenol in TPTX rats. These results suggest that catecholamine-induced hypercalcemia in TPTX rats is mediated by beta-2 adrenergic receptors. Related studies using rats prelabeled with 45Ca further suggest that the catecholamines, like parathyroid hormone, may act to raise blood calcium by mobilizing calcium from bone. The fact that these catecholamines could induce marked hypercalcemia in acutely TPTX rats but not in intact rats indicated that endogenous TCT protects the thyroid intact rat against hypercalcemia. The present findings support this idea in showing that isoproterenol and salbutamol raised levels of immunoreactive rat TCT in both thyroid venous and peripheral blood. Catecholamines apparently can promote TCT secretion, either directly or by a small transient increase in blood calcium. This, in turem, acts to combat hypercalcemia in thhroid-intact rats.

Albuterol↗