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At least 19 recordsLinked to original sources
PubMed1971

Lack of relationship between myocardial cyclic AMP concentrations and inotropic effects of sympathomimetic amines.

1. Sympathomimetic amines which increase the contractility of the isolated heart were tested for effects on cyclic AMP concentrations in rabbit heart slices and on adenyl cyclase activity in rabbit heart homogenate.2. Noradrenaline, as expected, stimulated adenyl cyclase activity and increased cyclic AMP concentrations, but dopamine and phenylephrine were ineffective.3. This result does not support the concept that cyclic AMP plays an essential role in the inotropic effect of sympathomimetic amines.

Adenylyl Cyclases↗
PubMed2000

GC-MS identification of sympathomimetic amine drugs in urine: rapid methodology applicable for emergency clinical toxicology.

A method was developed that permitted rapid identification in urine of the following sympathomimetic amines: amphetamine, benzphetamine, cathinone, desmethylsegiline, diethylpropion, ephedrine, fenfluramine, mazindol, methylenedioxyamphetamine, methylenedioxyethylamphetamine, methylenedioxymethamphetamine, mescaline, methamphetamine, methcathinone, methylaminorex, methylphenidate, pemoline, phendimetrazine, phenylepherine, phentermine, phenylpropanolamine, pseudoephedrine, and selegiline. In addition, two alpha-phenylethylamine-like monoamine oxidase inhibitors, phenelizine and tranylcypromine, were studied. Those sympathomimetic amines containing a primary or secondary amine, a hydrazine, and/or hydroxyl (except mazindol) functional groups were derivatized effectively using an on-column derivatization technique that used a reagent consisting of 10% fluoroanhydride in hexane, whereas the other sympathomimetic amines, including mazindol, were analyzed underivatized. Three different fluoroanhydrides, trifluoroacetic (TFAA), pentafluoropropionic (PFPA), and heptafluorobutyric (HFBA), and three different injection-port temperatures (160, 200, and 260 degrees C) were investigated. Both TFAA and PFPA gave sympathomimetic amine derivatives with essentially identical retention times, whereas HFBA gave longer retention times and better separation of individual compounds. The base fragmentation ion was noted to increase 50 amu (CF2) for each derivatized sympathomimetic amine as the length of the carbon-fluorine chain increased. Fragmentation ion abundance was maximized at an injection-port temperature of 260 degrees C, and this enhanced sensitivity coupled with the better chromatographic resolution of the individual sympathomimetic amines prompted the selection of HFBA as the derivatizing agent of choice. Assignments were made for the fragmentation ions produced by each derivatized drug. The developed method was adapted to analyze urine specimens that might be encountered in emergency toxicology testing. For identification of sympathomimetic amines requiring derivatization, 0.1 mL of the patient specimen had amphetamine-d5 and methamphetamine-d5 added as internal standard followed by adjustment of pH to 9.3 with borate buffer, extraction with 9:1 chloroform/isopropanol, centrifugation and separation of the organic phase, addition of 10% methanolic HCI and evaporation under nitrogen, reconstitution with HFBA reagent, and on-column derivatization during gas chromatographic-mass spectrometric (GC-MS) analysis. For those sympathomimetic amines not requiring derivatization, 1.0 mL of urine specimen had diazepam-d5 added as internal standard followed by the same extraction procedure and reconstitution accomplished with ethyl acetate. Because precolumn derivatization was eliminated and only 8 min was required for GC-MS analysis, complete analysis time was approximately 30 min, making the method suitable for clinical emergency toxicology purposes.

Emergency Service, Hospital↗
PubMed1982

Sympathomimetic amines: potential clinical applications in ischemic heart disease.

Sympathomimetic amines are useful in the treatment of patients with ischemic heart disease complicated by heart failure and shock. These agents influence the cardiovascular system by action on alpha-adrenergic, beta-adrenergic, and dopamine receptors. Recent evidence has demonstrated the existence of subtypes of the classic adrenergic and dopamine receptors that mediate distinct physiologic effects. The relative actions of sympathomimetic amines on these receptors differ substantially, resulting in considerable variation in their cardiac and peripheral vascular effects. Two classes of sympathomimetic amines are being intensively investigated at present: (1) compounds acting predominantly on beta 1-adrenergic receptors (i.e., they increase cardiac contractile force with little or no peripheral vascular effects) and (2) compounds acting on both beta 1-adrenergic and dopamine receptors. Orally active compounds of these two classes have been synthesized recently and are now under study for the treatment of patients with heart failure. Results of preliminary studies with such components are briefly reviewed.

Animals↗
PubMed1977

Effect of acetyl derivatives of some sympathomimetic amines on the blood pressure of the rat.

The effect of five sympathomimetic amines and some of their acetyl derivatives on the blood pressure of the rat was determined on the left carotid artery. After pretreatment with chlorisondamine (1 mg/kg subcutaneously) the blood pressure rise by sympathomimetic amines and their acetyl derivatives was compared with that of adrenaline. If the potency of adrenaline is specified as 100, the potencies of the other drugs are phenylephrine (metaoxedrinum, NFN) 37, tyramine 1.1, O-acetyltyramine 0.52, amphetamine 0.50, O-diacetylphenylephrine 0.25, ephedrine 0.23, O-acetylephedrine 0.02, N-acetylphenylephrine 0.01. The effects of N-acetyltyramine, N-acetylephedrine and N-acetylamphetamine are even weaker. Reserpine 5.0 or 0.05 mg/kg intraperitoneally 24 hours before the experiment increased the blood pressure rise by the directly acting sympathomimetic amines and their acetyl derivatives, but decreased the effects of the indirectly acting drugs. After treatment with phenoxybenzamine (2 mg/kg intraperitoneally), adrenaline exhibited the greatest blood pressure decrease and the effects of the other drugs in descending order: orciprenaline, O-acetyltyramine, phenylephrine, ephedrine, amphetamine, O-diacetylphenylephrine and O-acetylephedrine. Tyramine did not show any blood pressure decrease. The blood pressure decrease by sympathomimetic amines and by their acetyl derivatives was probably due to beta-receptor stimulation because it was prevented by propranolol. The N-acetyl derivatives recembled their parent drugs with regard to the immediate onset and short duration of their effects. The O-acetyl derivatives exhibited slower onset and longer duration of effect than their parent drugs. Physostigmine-pretreatment diminished the rise in blood pressure by O-acetyltyramine, but the effect of tyramine remained unchanged.

Amphetamines↗
PubMed1976

Thin layer chromatographic identification of some sympathomimetic amines.

Thin layer chromatographic behavior of some sympathomimetic amines in the presence of acids in neutral and organic solvent systems is reported. The sympathomimetic amines were dissolved in 0.1N HCl or ethanol and treated with bromocresol green or p-nitrobenzoyl chloride reagents on fiber sheets or precoated glass plates. Two-, 3-, and 4-, component solvent systems were tested. Benzene-ethyl acetate gave 2 spots for each amine standard; the more polar spots were satisfactorily separated. Amines in pharmaccuticals were not separated by any solvent system tested.

Amines↗
PubMed1963

TACHYPHYLAXIS TO SOME SYMPATHOMIMETIC AMINES IN RELATION TO MONOAMINE OXIDASE.

Tachyphylaxis to the effects of indirectly acting sympathomimetic amines has been studied on the blood pressure of the cat, rabbit and rat, on the cat spleen and nictitating membrane and on the rabbit heart. The pressor responses to tyramine and to phenethylamine declined slowly with repeated injection; the extent of tachyphylaxis induced by these amines depended on the dosage and on the frequency of injection. The pressor responses to alpha-methyltyramine and to dexamphetamine (alpha-methylphenethylamine) declined rapidly with successive injections. The tachyphylaxis induced by one indirectly acting sympathomimetic amine is crossed to others, but not to directly acting amines, such as noradrenaline. In animals treated with nialamide, a drug which inhibits monoamine oxidase, the tachyphylaxis induced by tyramine and by phenethylamine was similar to that produced by their alpha-methyl derivatives in normal animals. Similar results were obtained when the responses to indirectly acting sympathomimetic amines were studied on the cat spleen in situ and on the rabbit heart in vitro. Indirectly acting sympathomimetic amines impaired the responses of the cat nictitating membrane to sympathetic nerve stimulation; this effect was most evident with alpha-methylated amines.

Animals↗
PubMed1969

Excitatory action of sympathomimetic amines on 5-hydroxytryptamine receptors of gut.

1. Twenty-two sympathomimetic amines were tested for excitatory activity on isolated guinea-pig ileum, rabbit jejunum, and rat stomach.2. Eight amines contracted all or almost all guinea-pig ileum preparations; five amines contracted half the preparations and relaxed the others. Nine amines were consistently relaxant. Structural requirements for excitatory activity were not clear.3. Six amines contracted rat stomach and only four contracted rabbit jejunum. Only beta-phenylethylamine and (-)-amphetamine contracted all three preparations.4. The excitatory effects of the sympathomimetic amines on guinea-pig ileum seem to be due to an action on 5-hydroxytryptamine receptors. This conclusion is based on evidence that their excitatory action is antagonized by 2-bromolysergic acid diethylamide, by morphine and by desensitization with 5-hydroxytryptamine, and that there is cross-protection between 5-hydroxytryptamine and the excitatory sympathomimetic amines against block by phenoxybenzamine.

Amphetamine↗
PubMedDate not supplied

Distinguishing sympathomimetic amines from amphetamine and methamphetamine in urine by gas chromatography/mass spectrometry.

Derivatives of seven commonly used sympathomimetic amines and two "designer amines" were isolated from urine, separated chromatographically from amphetamine and methamphetamine, and determined by mass spectrometry with selected ion monitoring. The drugs included ephedrine, propylhexedrine, pseudoephedrine, phenylpropanolamine, hydroxynorephedrine, phenylephrine, phentermine, methylenedioxyamphetamine (MDA), and methylenedioxy methamphetamine (MDMA). The drugs were liquid extracted from urine and derivatized by either heptafluorobutyric anhydride (HFBA) or 4-carbethoxyhexafluorobutyryl chloride (4-CB). Because the base peak ions for ephedrine, pseudoephedrine, propylhexedrine, MDMA, and phentermine are identical to methamphetamine (e.g. 254 amu for HFBA) and those for phenylephrine, hydroxynorephedrine, phenylpropanolamine, and MDA are identical to amphetamine (e.g. 240 amu for HFBA), a table of selected ions was developed for all 11 drugs that distinguished amphetamine and methamphetamine from the sympathomimetic amines with either HFBA or 4-CB. The distinguishing ions rely on the ring structure of the different drugs and fragmentation associated with that structure. The 4-CB reagent partially derivatized the hydroxy-containing sympathomimetic amines, while the HFBA completely derivatized all the sympathomimetic amines. Furthermore, false positive results for the 4-CB reagent were found only for methamphetamine (20-2250 ng/mL of methamphetamine) when high concentrations (greater than 5 micrograms) of ephedrine or pseudoephedrine were present in the specimen. These results are related to a combination of injection port temperature and cleanliness of the injection port sleeve.

Amphetamine↗
PubMed1977

Effect of acetylated derivatives of some sympathomimetic amines on the isolated auricles and tracheal chain of the guinea-pig.

The effects of acetylation of sympathomimetic amines, tyramine, amphetamine, ephedrine, phenylephrine, orciprenaline, and salbutamol, and their O- and N-acetyl derivatives and the effects of reserpine or physostigmine pretreatment on the isolated auricles and tracheal chain of guinea-pigs have been studied. All the parent drugs relaxed the tracheal chain and had a positive inotropic and chronotropic effect on the isolated auricles; only amphetamine, on the contrary, contracted the tracheal chain. O-acetylation of these sympathomimetic amines generally decreased less chronotropic than iontropic action on the isolated auricles. O-acetylation of tyramine however: actually increased the positive chronotropic activity of drug. As a rule, O-acetylation also decreased the beta-adrenergic effect of these compounds on the tracheal chain, but not so markedly as on the isolated auricles. N-acetylation generally abolished the adrenergic effects of these sympathomimetic amines on the isolated auricles and decreased those effects on the tracheal preparation. N,O-triacetylation of salbutamol abolished the stimulating effect of the parent drug on the auricles but increased the relaxant activity on the trachea. Physostigmine antagonized the effects of O-acetyltyramine and O-triacetylorciprenaline but not those of tyramine and orciprenaline on the trachea preparation. It is concluded that among the sympathomimetic amines acetylation may be utilized for the development of specific bronchodilators and O-acetylation for inducing drug latentiation.

Acetylation↗
PubMed1960

Effect of denervation and of cocaine on the action of sympathomimetic amines.

The secretory effect of sympathomimetic amines on the submaxillary gland of cats was increased after section of the chorda tympani (preganglionic, parasympathetic supply). After sympathetic denervation of the gland the secretory response to tyramine and phenylethylamine was absent, the response to dopamine and ephedrine decreased and the response to adrenaline and noradrenaline increased. Large doses of cocaine, given locally into the gland, produced changes similar to those observed after sympathetic denervation. The sensitization towards adrenaline and noradrenaline was obtained with smaller doses. Tyramine did not cause a release of catechols from the suprarenal glands of the cat.

Animals↗
PubMed1990

Sympathomimetic amines and cardiac arrhythmias.

STUDY OBJECTIVE: The aim was to investigate the arrhythmogenic properties of several sympathomimetic amines and their antagonism by adrenergic blocking drugs. DESIGN: Arrhythmia was induced by the investigated drugs, injected intravenously: adrenaline (ADR); noradrenaline (NA); phenylephrine (PE); isoprenaline (IP); terbutaline (Tb) and salbutamol (Sb). ADR and PE were also tested for their arrhythmogenic properties after the administration of the adrenergic antagonists propranolol, phentolamine, or both. The dose required to induce arrhythmia and the proportion of animals that developed arrhythmia at a given dose were recorded. SUBJECTS: 63 anaesthetised cats of either sex, weight 2.0-4.3 kg, were used. MEASUREMENTS AND RESULTS: The electrocardiogram was recorded continuously. The arrhythmogenic potency sequence (expressed as arrhythmogenic dose, AD50 in micrograms) was: ADR 16; NA 24; PE 75; IP 133; Tb 500; Sb greater than 1000. The arrhythmogenic efficacy (in %) was: ADR 97; NA 91; PE 90; IP 82; Tb 50; and Sb 0. Propranolol and phentolamine were both effective in reducing the arrhythmogenic effects of ADR and PE. However, their combined administration was most effective and abolished the arrhythmias. CONCLUSIONS: Arrhythmogenicity is a property of sympathomimetic amines with either alpha or beta adrenergic effects, but simultaneous activation of both types of receptors is required for maximal manifestations. Similarly, antagonism at both sites is necessary in order to abolish arrhythmias induced by sympathomimetic amines completely.

Adrenergic alpha-Antagonists↗
PubMed1974

Mechanism of the pro-inflammatory activity of sympathomimetic amines in thermic oedema of the rat paw.

1 Thermic oedema induced by heating rat paws at 46.5 degrees C was potentiated by local injection of adrenaline, noradrenaline or high doses of isoprenaline. The pro-inflammatory effect of sympathomimetic amines was antagonized by phenoxybenzamine or phentolamine but not by propranolol.2 The subcutaneous space of heated rat paws was perfused with Tyrode solution and the perfusate collected and assayed for bradykinin, bradykininogen, kinin-forming activity and kininase activity. When adrenaline (0.5 mug/ml) was included in the perfusion fluid, kininase activity of the perfusate was increased by 76% and free bradykinin reduced by 46%.3 Increased vascular permeability induced by injection of bradykinin or kallikrein was reduced by adrenaline or noradrenaline, but isoprenaline had no significant effect.4 Pretreatment with soya bean trypsin inhibitor (SBTI) or heparin did not antagonize the pro-inflammatory effect of adrenaline or thermic oedema per se.5 Potentiation of thermic oedema similar to that induced by sympathomimetic amines was obtained by injecting paws with vasopressin prior to heating, or by applying a ligature to stop blood flow to the paw for the first 15 min of heating.6 Thermistor probes inserted beneath the paw skin showed that sympathomimetic amines increased the internal temperature of heated paws. This was significant, as small changes in temperature had a marked effect on the development of thermic oedema.7 It is suggested that sympathomimetic amines potentiate thermic oedema of rat paws heated at 46.5 degrees C by reducing blood flow to the paw, thereby causing a greater rise in paw temperature and consequently greater injury.

Animals↗
PubMed1971

Inhibitory and excitatory effects of sympathomimetic amines on muscle strips from the stomach of the guinea-pig.

1. Responses of muscle strips from the stomach of the guinea-pig have been recorded. Sympathomimetic amines cause inhibitory, motor or biphasic responses.2. The motor components of the responses of the preparations were greatly enhanced by the removal of the mucosal layers.3. The inhibitory responses to isoprenaline, noradrenaline and phenylephrine were antagonized by propranolol or by sotalol. The inhibitory responses to noradrenaline and phenylephrine but not isoprenaline were antagonized by phentolamine. Therefore, both alpha- and beta-adrenoceptors may subserve inhibition.4. The motor responses to noradrenaline and phenylephrine were often potentiated by propranolol or sotalol and were antagonized by phentolamine. Therefore, motor responses to sympathomimetic amines appear to involve alpha-adrenoceptors.5. The responses to sympathomimetic amines and their antagonists were not modified by hyoscine or by tetrodotoxin. It is concluded that the adrenoceptors mediating the responses recorded from these preparations are located on the smooth muscle cells rather than on a nervous pathway.

Anilides↗
PubMed1982

Use of rapid superfusion to differentiate the release of dopamine from striatal tissue induced by sympathomimetic amines from release induced by potassium.

A rapid superfusion system incorporating a continuous amperometric detector has been employed to study the effects of p-tyramine, d-amphetamine and cocaine on K+-stimulated release of dopamine (DA) from striatal tissue. Qualitative identification of the released substances is made by liquid chromatography with electrochemical detection and DA is established to be the principal substance released following exposure of the tissue to 60 mM K+ in the presence of Ca++. At a superfusion rate of 1 ml/min with a 20 microliter volume tissue holder, d-amphetamine and p-tyramine do not elicit detectable release of endogenous substances. These results are in direct contrast to the significant release of DA observed when striatal tissue is incubated with d-amphetamine for the same time period and suggest that the pools susceptible to release by the sympathomimetic amines are removed by superfusion. When striatal tissue is superfused with a buffer containing 60 mM K+ and cocaine or sympathomimetic amines, the effects of uptake blockade are manifested as an increase in the amount and duration of observed release over that obtained with 60 mM K+. In a competitive study of cocaine and p-tyramine with d-amphetamine, it appears that all three of these agents induce blockade at the same site(s). All of these data are in direct accord with the facilitated exchange diffusion mechanism proposed for the actions of sympathomimetic amines at DA nerve terminals.

Animals↗
PubMed1969

Effects of a haloalkylamine on responses to and disposition of sympathomimetic amines.

1. The mechanisms by which a haloalkylamine (GD-131) alters the inactivation of and potentiates responses to certain sympathomimetic amines, and the relationship of these actions to the similar effects of cocaine were investigated in rabbit aortic strips. The technique of oil immersion was used to assess rates of amine inactivation.2. Exposures to GD-131, which produced no detectable alpha-adrenergic blockade, markedly slowed the inactivation of noradrenaline. It was concluded that it is unnecessary to postulate a role of adrenergic receptors in the inactivation of catecholamines to account for the reported effects of haloalkylamines on amine output during adrenergic nerve stimulation.3. The reduction in the rate of noradrenaline inactivation produced by moderate exposure to GD-131 was approximately equivalent to that due to inhibition of both monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT). Addition of GD-131 did not further slow inactivation in preparations in which MAO and COMT had been inhibited, but the effects of both GD-131 and of enzyme inhibition on noradrenaline disposition were additive with that of cocaine.4. Cocaine consistently inhibited and GD-131 markedly potentiated responses to tyramine. The augmentation of responses by GD-131 was much greater than could be accounted for by the slight release of endogenous catecholamine by this agent. Thus the principal effect of the haloalkylamine appears not to involve inhibition of nerve cell membrane transport of amine.5. Maximal exposure to GD-131 short of that which produced alpha-adrenergic blockade sometimes slowed the inactivation of noradrenaline as much as did inhibition of both MAO and COMT plus the maximal effect of cocaine.6. These results seem best explained by postulating that GD-131 and other haloalkylamines inhibit the passage of sympathomimetic amines through biological membranes. Passage to sites of enzymatic inactivation, predominantly in non-neuronal tissue, is most readily inhibited. The "cocaine-sensitive mechanism," transport to sites of binding and storage, can also be inhibited, but is considerably less sensitive.7. GD-131 potentiated responses to noradrenaline more than did the maximally effective concentration of cocaine. Cocaine produced very little additional potentiation when added in the presence of GD-131, whereas the latter had a reduced, but still significant effect in the presence of cocaine. Most of the effect of cocaine and at least half of that of GD-131 was due to a common action on effector cells, which is unrelated to any alteration of amine disposition. The balance of the potentiation by GD-131 may be due to inhibition of access of amine to sites of enzymatic inactivation, perhaps involving a reduction in the volume of distribution in intracellular water, and a very small part of the potentiation by cocaine may be secondary to inhibition of transport of amine to sites of binding and storage.8. On the basis of the present observations, it is postulated that a major part of the noradrenaline released by adrenergic nerve activity is involved in the activation of tissue receptors and has its action terminated by movement away from the region of the receptors. A small portion of the mediator is removed by the circulation, some is taken up by adrenergic nerves, but the major part enters non-nervous cells and is distributed in intracellular water. The capacity of this intracellular compartment appears to be limited and enzymatic inactivation is essential to maintain its function. O-methylation is the dominant primary enzymatic process in the inactivation of physiological amounts of noradrenaline, but MAO appears to function "in series" as an effective alternate pathway of disposition.

Amines↗