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At least 1,477 records · Page 82Linked to original sources
PubMed1986

A method for presenting and comparing dose-response curves.

When dose-response curves are replicated, averaging the responses to each dose of drug reduces the slope of the mean curve. The shape of the curve can be preserved, however, by first normalizing each dose-response curve and then interpolating log concentrations that induce predetermined responses. These log concentrations are averaged, and then the responses are scaled to the mean maximal response. Mean dose-response curves obtained using this method were compared with mean curves obtained by the conventional method. It was found that this method did not distort the slope of the curve, and smaller differences were detected as significant. Neither method was found to be satisfactory for obtaining a truly representative mean curve for biphasic dose-response curves. The nature of the distribution of EC50 and maximal response was investigated, and it was confirmed that EC50 are log-normally distributed, whereas maximal responses are normally distributed.

Adrenergic beta-Antagonists↗
PubMed1983

Electrophysiologic properties of prenalterol.

We assessed the electrophysiological properties of prenalterol, a new beta-selective agonist, in 10 patients with normal and 10 patients with delayed atrioventricular (A-V) conduction times. We evaluated sinus node function, A-V conduction times, refractory periods, atrial or ventricular arrhythmias, spontaneous or induced by the single extrastimulus technique during basal conditions, 5 minutes after a first dose of 20 micrograms/kg of prenalterol, and 5, 15 and 30 minutes after a second injection of the same dose. Prenalterol increased heart rate about 20%, with statistically significant shortening of right atrial refractory periods, A-V nodal functional and effective refractory periods and A-H interval in both groups after the first dose. In the 6 patients with sick sinus syndrome, prenalterol increased heart rate significantly and decreased maximum sinus node recovery time which reached a statistically significant value (P less than 0.05) 5 and 30 minutes after the second dose. At the highest dose, prenalterol seemed to increase the number of ventricular and/or atrial arrhythmias only in those patients with the arrhythmias before treatment. Prenalterol increases heart rate and decreases A-V node conduction times. The shortening of maximum sinus node recovery time in patients with the sick sinus syndrome, especially if confirmed after oral administration, could indicate a specific use of this drug in patients with sinus bradycardia or atrial fibrillation with a slow ventricular response.

Adrenergic beta-Agonists↗
PubMed1986

A toxicological review of beta-adrenergic blockers.

The use of various beta-adrenergic blockers has become extensive as they have been found to be efficacious in the treatment of a number of cardiovascular problems including cardiac arrhythmias, angina pectoris, and hypertension. The widespread and chronic use of these drugs has generated a concern for their potential chronic toxicity. Eighteen beta-adrenergic blockers have been reviewed and the available literature pertaining to their potential carcinogenicity, mutagenicity, and teratogenicity has been summarized and compared.

Acebutolol↗
PubMed1984

Old and new inotropic drugs.

An ideal cardiotonic agent should improve cardiac contractility and increase the oxygen supply to various tissues without inducing tachycardia, arrhythmias, decrease in coronary blood flow or increment in oxygen requirements of the myocardium. It should also be safe and orally active and have a persistent action. The aim of this paper is to describe various positive inotropic drugs at our disposal. The hemodynamic effects and the indications of adrenaline, noradrenaline, isoprenaline, dopamine, dobutamine and cardiac glycosides are presented first. Then several new promising orally active compounds are discussed.

Adrenergic beta-Agonists↗
PubMed1986

Adrenergic and serotonergic regulation of skeletal muscle metabolism in the rat: specificity of the serotonin- and isoproterenol-stimulable adenylyl cyclase in sarcolemma.

The specificity and kinetics of rat sarcolemmal serotonin- and isoproterenol-stimulable adenylyl cyclases were studied. The stimulation of adenylyl cyclase by serotonin was less than that by isoproterenol and required low concentrations of ATP (0.1 mM), 10 microM GTP, and free Mg ion concentrations of 10-20 microM. The isoproterenol-stimulated activity was readily detectable over a much wider range of MgCl2 (1.0-5.0 mM) and ATP (0.1-3.0 mM). (+/-)-Oxprenolol and l(-)-propranolol inhibited isoproterenol stimulation with KB values of 6.3 X 10(-9) M and 1.9 X 10(-9) M, respectively. Interference by (+/-)-cyproheptadine, (+/-)-methysergide and d(+)-propranolol was not strictly competitive. However, these were much more potent inhibitors of serotonin stimulation than were oxprenolol and l-propranolol. The concentrations of antagonists producing 50% inhibition (IC50) of the maximal adenylyl cyclase stimulation by serotonin were compared to the IC50 obtained with isoproterenol; the ratios were 0.02 for oxprenolol, 0.50 for l-propranolol, 295 for d-propranolol, 2438 for cyproheptadine, 578 for methysergide and greater than 125,000 for lysergic acid diethylamide (LSD). These data indicate that rat skeletal muscle adenylyl is stimulated by discrete serotonergic and adrenergic receptors, and that there may be distinct conditions for optional stimulation.

Adenylyl Cyclases↗
PubMed2005

Liquid-phase microextraction based on carrier mediated transport combined with liquid chromatography-mass spectrometry. New concept for the determination of polar drugs in a single drop of human plasma.

Recently, we demonstrated for the first time liquid-phase microextraction (LPME) of polar drugs based on carrier mediated transport. In this new extraction technique, selected analytes were extracted as ion-pairs from small volumes of biological samples, through a thin layer of a water immiscible organic solvent immobilised in the pores of a porous hollow fibre (liquid membrane), and into a microl volume of an acidic aqueous acceptor solution placed inside the lumen of the hollow fibre. In the current paper, this new extraction technique was combined with liquid chromatography-mass spectrometry (LC-MS) for the first time. Carrier mediated LPME was evaluated for several new model drugs (0.01 <log P< 1.76), the sample clean-up aspects were investigated in detail, and this new extraction technique was fully validated for the first time. Extractions were performed from 50 microl of human plasma samples, which provided sufficient material in combination with LC-MS. Sodium octanoate (50 mM) was added to the sample as carrier, 1-octanol (approximately 15 microl) was used as the liquid membrane in the wall of the hollow fibre, and 50 mM HCl was utilized as acceptor solution in the lumen of the hollow fibre. The addition of carrier to the samples was found to significantly improve extraction recoveries for the polar drugs tested, providing recoveries in the range 16-78%. Validation was accomplished for atenolol and cimetidine. Limits of quantification (S/N = 5) from 50 microl of plasma were 25 and 50 ng/ml for atenolol and cimetidine, respectively. The intra-day precision (R.S.D.) ranged from 7.8 to 17.2% and from 9.5 to 14.1% for atenolol and cimetidine, respectively, and corresponding inter-day precisions (R.S.D.) were within 6.7-1.4% and 7.7-20.3%. The method was linear in the range 25-1500 ng/ml for atenolol (r = 0.992), and 50-3500 ng/ml for cimetidine (r = 0.976). The accuracy of the method was found to be in range 89.1-99.6% and 83.4-86% for atenolol and cimetidine, respectively. The sample clean-up obtained by carrier mediated LPME was excellent, providing a significantly lower back-ground level in total ion current chromatograms by LC-MS as compared to protein precipitation.

Amphetamine↗
PubMed1999

Constitutively active mutants of the beta1-adrenergic receptor.

We provide the first evidence that point mutations can constitutively activate the beta(1)-adrenergic receptor (AR). Leucine 322 of the beta(1)-AR in the C-terminal portion of its third intracellular loop was replaced with seven amino acids (I, T, E, F, C, A and K) differing in their physico-chemical properties. The beta(1)-AR mutants expressed in HEK-293 cells displayed various levels of constitutive activity which could be partially inhibited by some beta-blockers. The results of this study might have interesting implications for future studies aiming at elucidating the activation process of the beta(1)-AR as well as the mechanism of action of beta-blockers.

Adrenergic beta-1 Receptor Agonists↗