PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SYMPATHOMIMETIC AMINES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1987

Mechanism of action of indirectly acting sympathomimetic amines.

The mode of action of indirectly acting sympathomimetic amines was analysed in the rat vas deferens (preloaded with 3H-(-)-noradrenaline). When monoamine oxidase (MAO), catechol-O-methyltransferase and vesicular uptake were inhibited (i.e., when the concentration of 3H-noradrenaline in the axoplasm was high), all substrates of neuronal uptake induced a carrier-mediated outward transport of 3H-noradrenaline, in strict dependence on the Km for neuronal uptake of the substrate. However, when MAO and vesicular uptake were not inhibited, some of the substrates of neuronal uptake were better releasers of 3H-noradrenaline than others; obviously, when the axoplasmic 3H-noradrenaline concentration is very low (intact vesicular uptake, intact MAO), a 'mobilization' of vesicular 3H-noradrenaline is a prerequisite for substantial release.

Animals↗
PubMed1990

Naloxone potentiation of cardiovascular responses to sympathomimetic amines in the rat.

The work was aimed at analyzing the ability of naloxone to potentiate 1) the arterial pressure responses to sympathomimetic amines administered i.v. in normotensive anesthetized, pithed, chemically sympathectomized or acutely adrenalectomized rats and 2) the chronotropic responses to norepinephrine in the isolated rat atria. In anesthetized rats, naloxone (2.5-10 mg/kg i.v.) potentiated the pressor responses to epinephrine (2 micrograms/kg). Naloxone (5 mg/kg) significantly potentiated the pressor responses to norepinephrine (1-4 micrograms/kg), phenylephrine (10-50 micrograms/kg) and the reflex pressor responses to a 60-sec carotid occlusion. On the contrary, naloxone did not potentiate the arterial pressure responses to methoxamine (100 micrograms/kg), angiotensin (0.5-2 micrograms/kg) and isoproterenol (1 micrograms/kg). Pithing or acute adrenalectomy did not alter the naloxone-induced potentiation of the pressor responses to norepinephrine (0.125-0.5 micrograms/kg). 6-Hydroxydopamine pretreatment abolished completely the naloxone-induced potentiation of the pressor responses to norepinephrine (0.25-1 micrograms/kg). In isolated rat atria, naloxone (1.4 and 2.8 x 10(-5) M) potentiated the chronotropic responses to norepinephrine (1.5-6 x 10(-8) M). It is suggested that naloxone potentiates cardiovascular responses to sympathomimetic amines by interacting with presynaptic adrenergic mechanisms which could additionally contribute to its pressor effects in acute hypotensive conditions.

Angiotensins↗
PubMed1977

Evoked efflux of 3H-bretylium by sympathomimetic amines from the rat vas deferens in vitro.

The efflux of 3H-bretylium in rat vas deferens in vitro evoked by a number of sympathomimetic amines was examined. The tissue was preloaded with 3H-bretylium (2 x 10(-7) M) and the efflux of bretylium to the incubation medium in the presence of the amines during 20 min, was determined. The efflux evoked by (+)-amphetamine was almost abolished at 0 degrees and by desipramine. The dose response curves showed that some of the amines at high concentrations markedly antagonized their own effect. It could be demonstrated that (+)-amphetamine and N-methylamphetamine at a high concentration also antagonized the efflux evoked by low external Na+ concentrations and it is suggested that this effect is produced by inhibition of the outward transport of bretylium through the neurone membrane. The structure activity relationship obtained shows that the non-hydroxylated amines are most potent in evoking bretylium efflux and that the potency diminished with the number of hydroxyl groups. The tertiary amine analogue of amphetamine is less active and the quaternary derivative much less active than amphetamine and N-methylamphetamine. A hydroxyl group at 3-position gives a somewhat higher potency than that at 4-position. This structure activity relationship is similar to that previously reported for the sympathomimetic amines in reversing the adrenergic neurone blockade for bretylium and it is proposed that this reversal is induced by the reduction of the intraneuronal concentration of bretylium as a result of the evoked efflux.

Amphetamine↗
PubMed1980

Sympathomimetic amines.

The autonomic nervous system may play an important role in tissue autoregulation as the neurohumoral transmission process has been shown to constitute the final common pathway by which the effects of many physiological and pharmacological substances are mediated. The effects of the administration of a sympathomimetic amine cannot be accurately predicted in a subject. Choice of which sympathomimetic amine to use should be determined on the basis of data obtained in relevant clinical circumstances, but the dose should always be titrated against the effect in each individual. It is interesting that adrenaline, "the original autonomic drug" with its "venerable history", is still a first line drug in many of the situations for which it was being prescribed in 1907. It is the drug of first choice in anaphylactic reactions and for severe allergic bronchospasm, and is widely used as a vasoconstrictor in surgery and with local anaesthetic agents. Adrenaline in "physiological" doses is a satisfactory and cheap alternative to other available drugs for use in septic shock and in emergence from cardiopulmonary bypass.

Action Potentials↗
PubMed1976

Sympathomimetic amines having a carbostyril nucleus.

A series of new sympathomimetic amines containing an 8-hydroxycarbostyril moiety was synthesized. These compounds probably exist as resonance hybrids having two acidic hydrogen atoms in locations approximating to those of the hydroxyl groups of catechol-containing adrenergic agents. In an in vitro test, many of these compounds showed potent activity for relaxation of guinea pig tracheal smooth muscle. One of the compounds was 24 000 times more potent than isoproterenol. Their actions on cardiac muscle were also examined in vitro by measuring increase in the beating rate of the right atria of guinea pigs. Several of the compounds appeared to be beta-selective. Some of the compounds seem suitable for use as bronchodilators. The structure-activity relationships of these compounds were discussed in comparison with those of catecholamines.

Adrenergic beta-Agonists↗
PubMed1962

Effect of sympathomimetic amines on the blocking action of guanethidine, bretylium and xylocholine.

Experiments were carried out in which the adrenergic neurone blocking activity of xylocholine, bretylium and guanethidine was studied by the use of the inhibitory responses of the isolated rabbit ileum to lumbar sympathetic nerve stimulation, and the contractions of the nictitating membrane of the anaesthetized cat in response to stimulation of the cervical sympathetic nerves. In both these preparations, after blockade of the effects of sympathetic nerve stimulation had been produced with xylocholine, bretylium or guanethicdine, the sympathomimetic amines, dexamphetamine, mephentermine, hydroxyamphetamine, ephedrine and phenethylamine, reversed the blockade; if these amines were given first, then the adrenergic neurone blocking agents were ineffective. Tyramine and dopamine were effective on the isolated rabbit ileum but not on the cat's nictitating membrane. Effective antagonism of the adrenergic neurone blocking drugs was also shown by some substances which inhibit mono-amine oxidase but only those which in addition possess sympathomimetic effects. Thus phenelzine, pheniprazine and tranylcypromine were effective whereas iproniazid and nialamide were not. Since xylocholine, bretylium and guanethidine were all antagonized by the same agents, it seems likely that they all produce sympathetic blockade by a similar mechanism. The possibility is discussed that the sympathomimetic amines which antagonize the adrenergic neurone blocking drugs are competing with these substances for the same receptor sites.

Amidines↗
PubMed1980

The effects of beta-sympathomimetic amines and phosphodiesterase inhibitors on electrophysiological parameters in Purkinje fibres.

Dose-dependent responses to L-isoprenaline of spontaneous activity and plateau height in Purkinje fibres can be mimicked closely by the PDE-inhibitor IBMX. Simultaneous applications of sympathomimetic amines and IBMX result in potentiated responses. The results support the hypothesis that cyclic-AMP is the common mediator of positive chronotropic and inotropic effects induced by beta-sympathomimetic amines.

1-Methyl-3-isobutylxanthine↗
PubMed1976

alpha-Adrenoceptors mediating positive inotropic effects on the ventricular myocardium: some aspects of structure-activity relationship of sympathomimetic amines.

Experiments were carried out on the isolated papillary muscle of the rabbit in order to further characterize the alpha-adrenoceptors mediating the positive inotropic effect. For this purpose dose-response relations of seven sympathomimetic amines were compared under the influence of alpha- and/or beta-adrenolytic drugs. Phentolamine (10(-6) M) shifted the lower part of the dose-response curves for norfenephrine, synephrine and epinine as for phenylephrine and adrenaline to the right, while prindolol (10(-8) M) affected only the upper part of the curves. In the presence of both alpha- and beta-adrenoceptor blocking agents the entire dose-response curves for sympathomimetic amines were shifted in a parallel manner. Noradrenaline affected preferentially beta-adrenoceptors, whereas its effect on alpha-adrenoceptors was so weak that it could be detected only when the neuronal and extraneuronal uptake mechanism of amines were blocked by cocaine (3 X 10(-5) M) and corticosterone (4 X 10(-5) M), respectively. The effect of dopamine was not affected either by phentolamine or by prindolol, but was antagonized by the simultaneous application of both alpha- and beta-adrenoceptor blocking agents. From the present results, it appears that the following relationships are present between the structure of amines and the alpha-adrenoceptor stimulating activity in the heart: (1) N-methylation increases the potency: (2) Absence of the hydroxyl group either in 3 or in 4 position decreases the intrinsic and beta-adrenoceptor stimulating activities, but increases the alpha-adrenoceptor stimulating activity.

Adrenergic alpha-Agonists↗
PubMed1975

The effect of cocaine, reserpine, and 6-hydroxydopamine on the response of the perfused central artery of the rabbit ear to sympathomimetic amines.

The perfused central artery of the rabbit ear was less sensitive to extraluminal than to intraluminal noradrenaline, but the reverse was true for metaraminol, methoxamine, metanephrine, and isoproterenol. No difference was noted between the extraluminal and intraluminal potency of phenylephrine. Cocaine potentiated the effect of extraluminal and intraluminal noradrenaline, but decreased that of intraluminal phenylephrine. Irrespective of the route of administration, the constrictor potencies of the sympathomimetic amines were not affected by cocaine. Arteries of reserpine-treated rabbits were supersensitive to extraluminally and intraluminally applied noradrenaline and phenylephrine, but they were not supersensitive to metaraminol. 6-Hydroxydopamine effectively destroyed adrenergic nerve endings of the central ear artery and increased its responses to both extraluminal and intraluminal noradrenaline and phenylephrine. However, only the constrictor potencies of intraluminally applied metaraminol and methoxamine were enhanced by 6-hydroxydopamine. The apparent discrepancies between the results obtained by various procedures that eliminate or impair the nerve uptake process suggest that the difference in the constrictor potency of extraluminal and intraluminal sympathomimetic amines is probably unrelated to their uptake by nerves located in the adventitio-medial junction of the artery.

Animals↗
PubMedDate not supplied

Hemodynamic effects of long term feeding of sympathomimetic amines to swine.

The hemodynamic effects of long term feeding of sympathomimetic amines (SPMA) to swine were studied. Three groups of female swine (N = 20 for each group) were fed either aminorex fumarate, d-amphetamine sulfate, or dextrose (control) for as long as 8 months in dosages up to 15 mg/kg/day. After 4 months of this feeding regiment, the weight gain of the pigs fed either aminorex or amphetamine was significantly less than the control animals. Hemodynamic measurements on awake swine indicated no elevation of pulmonary arterial blood pressure in the pigs fed SPMA. Measurement of systemic hemodynamics revealed that cardiac index was lower in the treated pigs than in control animals, but that heart rate and systemic arterial blood pressure were not altered by the drugs. In addition to baseline measurements of hemodynamic variables, the animals were exposed to acute hypoxia (12 percent O2 in N2) for 5 minutes. Although pulmonary arterial blood pressure increased similarly in the 3 groups of pigs, total pulmonary resistance increased to a greater extent in the pigs fed SPMA, indicating perhaps an enhancement of the hypoxic pulmonary pressor response after chronic ingestion of either amphetamine or aminorex. In a limited number of pigs, SPMA were fed for a period of 8 months, of which the last 3 months were during pregnancy. Hemodynamic measurements on sedated (metomidate, IV) swine revealed no difference in pulmonary arterial blood pressures between treated and control animals. We conclude that chronic ingestion of large doses of aminorex or amphetamine in swine does not lead to pulmonary arterial hypertension, but that slight reductions in cardiac output and subtle alterations in the pulmonary pressor response to acute hypoxia may occur.

Aminorex↗
PubMed1976

Centrally mediated cardiovascular responses to intracisternal injections of sympathomimetic amines in anesthetized rats.

The cardiovascular effects resulting from intracisternal (i.c.) injections of sympathomimetic amines were studied in alpha-chloralose-urethanized rats. Norepinephrine (0.5-5 mug i.c.) caused a typical rise in blood pressure with no significant change in heart rate and a fall in blood pressure with a bradycardia, which were completely blocked after treatment with phentolamine (10-50 mug i.c.) L-isoproterenol (0.05-0.5 mug i.c.) and trimetoquinol (0.5-3 mug i.c.), a beta-sympathomimetic agent, usually caused a fall in blood pressure with a tachycardia, which was reduced after treatment with propranolol (10-50 mug i.c.), but trimetoquinol was inclined to cause a rise in blood pressure with a tachycardia. Epinephrine (5 mug i.c.) showed both centrally mediated alpha- and beta-sympathomimetic effects. Tyramine (0.5-1 mg i.c.) caused mixed blood pressure responses presumably due to a release of norepinephrine and epinephrine, and these responses were partially blocked after treatment with phentolamine (100 mug i.c.) or propranolol (50 mug i.c.). These observations suggest that both alpha- and beta-sensitive adrenergic zones may exist on the vasomotor center of the pons and medulla in rats, and both norepinephrine and epinephrine might centrally play a physiological role as the neurotransmitters controlling blood pressure in rats.

Animals↗
PubMed1968

The effects of intracerebroventricularly administered noradnamine and other sympathomimetic amines upon leptazol convulsions in mice.

1. The influence of some intracerebroventricularly administered sympathomimetic amines on leptazol-induced convulsions has been investigated.2. Noradnamine and high doses of dopamine proved to be anticonvulsant and also antagonized the facilitative effects of reserpine.3. Noradrenaline and octopamine also antagonized reserpine-induced facilitation but were without effect on leptazol alone; by contrast tyramine and small doses of dopamine lowered the threshold for leptazol convulsions.4. A possible interpretation of these results is presented.

Animals↗
PubMed2001

Separation of sympathomimetic amines of abuse and related compounds by micellar electrokinetic chromatography.

Separation of twelve sympathomimetic amines and related compounds by micellar electrokinetic chromatography (MEKC) with UV absorbance detection is described. These amines were well separated within 25 min using 50 mM sodium tetraborate solution containing 15 mM sodium dodecylsulfate (SDS) of pH 9.3 as a running solution and detected at 210 nm. MEKC was performed with an applied voltage of 13 kV at 25 degrees C using a fused-silica capillary (50 cm x 75 mm i.d.) with effective length of 37.5 cm. The detection limits of these compounds were in the range from 4 to 97 fmol/injection at a signal-to-noise ratio (S/N) of 3. The reproducibility of the method expressed as relative standard deviation (RSD) for within-day (n=6) and between-day (n=5) assays was less than 4.8 and 8.8%, respectively. The proposed method could be applied to the determination of an anorectic drug, phentermine, in Chinese tea with a detection limit of 99 microg/g (105 fmol/injection, S/N=3).

Calibration↗
PubMed1980

Potentiative effects of alpha agonistic sympathomimetic amines on vasoconstriction by adrenergic nerve stimulation.

The effects of catecholamines and other sympathomimetic amines with alpha adrenergic activity on vasoconstriction were studied. Short ring segments were prepared from five rabbit blood vessels including the mesoduodenal, brachial, central ear and pulmonary lobar arteries and the saphenous vein. Constriction was elicited by electrical field stimulation of adrenergic neurons. This response was markedly potentiated in the mesenteric preparation by low concentrations of norepinephrine, epinephrine, phenylephrine, methoxamine, naphazoline and oxymetazoline. The potentiation occurred with amine concentrations not sufficient to elevate the spontaneous transmitter release or basal smooth muscle tone. Propranolol, cocaine and metanephrine did not prevent the potentiation. Isoproterenol and dopamine potentiated the response only in high concentrations and tyrosine was without an effect. An unidentified extraneuronal action was probably responsible for the potentiation. The mesenteric artery was unique for its marked potentiation as the brachial artery was potentiated only slightly and the other three vessels were inhibited by the alpha adrenergic agents in the constrictor response to stimulation.

Adrenergic alpha-Agonists↗
PubMed1977

Effect of sympathomimetic amines on the synaptosomal transport of noradrenaline, dopamine and 5-hydroxytryptamine.

The interaction of sympathomimetic amines with the transport of 3H-noradrenaline (3H-NE), 3H-dopamine (3H-DA) and 3H-5-hydroxytryptamine (3H-5-HT) were investigated in rat hypothalamic (3H-NE) and striatal (3H-DA) and 3 H-5-HT) synaptosomes. Modifications in the phenylethylamine structure led to changes in activity towards biogenic amine uptake and release: (a) the introduction of a beta-OH group led to compounds less active in inhibiting uptake and stimulating release of 3H-NE, 3H-DA and 3H-5-HT, with the exception of 3H-NE release which was stimulated more by unlabeled 1-NE than by DA; (b) the introduction of phenolic-OH groups always led to compounds which were stronger uptake inhibitors and releasers of the three biogenic amines; (c) the alpha-methylation increased the potency towards uptake inhibition and release stimulation, with the exception of 3H-NE release: in fact, the releasing activity of phenylethylamine was suppressed by alpha-methylation; (d) the introduction of a -Cl group in the para position selectively potentiated the effects on 3H-5-HT uptake and release and generally depressed those on catecholamine transport.

Animals↗
PubMed1979

Functional antagonism as a means of determining dissociation constants and relative efficacies of sympathomimetic amines in guinea-pig isolated atria.

1 The positive inotropic and chronotropic responses to sympathomimetic amines were examined in guinea-pig isolated atria. 2 The order of potency measured from EC50 values was isoprenaline greater than orciprenaline greater than salbutamol greater than or equal to fenoterol greater than terbutaline. Terbutaline and salbutamol were partial agonists on rate and together with orciprenaline and fenoterol also on tension responses. 3 Functional antagonism by carbachol caused a rightwards shift of the dose-response curve and depression of the maximum response. The rate maxima for orciprenaline, fenoterol and terbutaline were above that of isoprenaline. All the tension maxima were below isoprenaline. 4 Dissociation constants (KA) and relative efficacies (er) were determined by analogy with irreversible antagonism. 5 The relative orders of affinity (KA) were isoprenaline greater than orciprenaline greater than fenoterol greater than salbutamol greater than terbutaline. Affinities were identical on rate and tension. 6 The relative efficacies were all greater than isoprenaline for rate responses. On tension they were the same or less than isoprenaline. 7 The implications of these results are discussed, in particular the fact that a partial agonist has a greater efficacy than a full agonist.

Animals↗
PubMed1985

Mechanisms of supersensitivity to sympathomimetic amines in the chronically denervated heart of the conscious dog.

Mechanisms of denervation supersensitivity to sympathomimetic amines were studied in conscious animals. Norepinephrine, 0.1 micrograms/kg, increased left ventricular dP/dt significantly more (4208 +/- 828 mm Hg/sec) in dogs with cardiac denervation than in intact dogs (1029 +/- 280 mm Hg/sec), P less than 0.01, whereas responses to isoproterenol were similar in both groups. Denervation supersensitivity to isoproterenol could be demonstrated only after opposing reflex effects were blocked. After ganglionic blockade, norepinephrine still induced 2- to 3-fold greater increases in left ventricular dP/dt and 3- to 7-fold greater increases in heart rate in cardiac-denervated dogs, whereas isoproterenol and prenalterol, not taken up by presynaptic nerve endings, elicited only 40%-50% greater increases in left ventricular dP/dt and heart rate in dogs with cardiac denervation. The density of beta-adrenergic receptors [( 3H]dihydroalprenolol) was elevated (P less than 0.01) in denervated left ventricles (105 +/- 6.9 fmol/mg protein, n = 8) compared to normal left ventricles (70 +/- 6.3 fmol/mg protein, n = 12). This was accompanied by enhanced isoproterenol-mediated adenylate cyclase activity. However, muscarinic cholinergic receptor density, [( 3H]quinuclidinyl benzilate), decreased from control levels of 251 +/- 11 fmol/mg protein (n = 7) to 193 +/- 14 fmol/mg protein (n = 6). Thus, chronic cardiac denervation results in upregulation of the beta-adrenergic receptor and down-regulation of the muscarinic receptor. The increased beta-adrenergic receptor density and adenylate cyclase stimulation correlated well with the amount of denervation supersensitivity to isoproterenol and prenalterol, but accounted for only a minor fraction of denervation supersensitivity to norepinephrine. The major mechanism of denervation supersensitivity to norepinephrine appears to involve lack of the norepinephrine reuptake.

Adenylyl Cyclases↗