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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↗
PubMed1999

Sympathomimetic effects of MIBG: comparison with tyramine.

UNLABELLED: Because nothing is known about whether metaiodobenzylguanidine (MIBG) has tyramine-like actions, the sympathomimetic effects of MIBG were determined in the isolated rabbit heart and compared with those of tyramine. METHODS: Spontaneously beating rabbit hearts were perfused with Tyrode's solution (Langendorff technique; 37 degrees C; 26 mL/min), and the heart rate as well as the norepinephrine and dopamine overflow into the perfusate was measured before and after doses of MIBG or tyramine (0.03-10 micromol) given as bolus injections (100 microL) into the aortic cannula. Km and Vmax values for the neuronal uptake (uptake1) of 125I-MIBG and 14C-tyramine were obtained in human neuroblastoma (SK-N-SH) cells. The Ki of MIBG for inhibition of the 3H-catecholamine uptake mediated by the vesicular monoamine transporter was determined in membrane vesicles obtained from bovine chromaffin granules and compared with the previously reported Ki value for tyramine determined under identical experimental conditions. RESULTS: By producing increases in heart rate and norepinephrine overflow, both compounds had dose-dependent sympathomimetic effects in the rabbit heart. MIBG was much less effective than tyramine in increasing heart rate (maximum effect 59 versus 156 beats/min) and norepinephrine overflow (maximum effect 35 versus 218 pmol/g). Tyramine also caused increases in dopamine overflow, whereas MIBG was a poor dopamine releaser. At a dose of 10 micromol, the increase in heart rate lasted more than 60 min after MIBG and about 20 min after tyramine injection. Accordingly, the norepinephrine overflow caused by 10 micromol MIBG and tyramine declined with half-lives of 57.8 and 2.2 min, respectively. The effects of both drugs were drastically reduced in hearts exposed to 2 micromol/L desipramine. The kinetic parameters characterizing the saturation of neuronal uptake by 125I-MIBG and 14C-tyramine were similar for the two compounds: Km values of MIBG and tyramine were 1.6 and 1.7 micromol/L, respectively, and Vmax values of MIBG and tyramine were 43 and 37 pmol/mg protein/min, respectively. However, in inhibiting the vesicular 3H-catecholamine uptake, MIBG was eight times less potent than tyramine. CONCLUSION: MIBG is much less effective than tyramine as an indirect sympathomimetic agent. This is probably a result of its relatively low affinity for the vesicular monoamine transporter and explains the relatively poor ability of the drug to mobilize norepinephrine stored in synaptic vesicles. The long duration of MIBG action results primarily from the drug not being metabolized by monoamine oxidase. The sympathomimetic effects of MIBG described here are not likely to come into play in patients given diagnostic or common therapeutic doses of radioiodinated MIBG.

3-Iodobenzylguanidine↗
PubMed1992

Highly potent beta-2 sympathomimetics convert to less potent partial agonists as relaxants of guinea pig tracheae maximally contracted by carbachol. Comparison of relaxation with receptor binding and adenylate cyclase stimulation.

Beta-adrenergic agonists are among to the most potent dilators of airway smooth muscle available and act as functional antagonists of a variety of contractile stimuli. In order to elucidate their loss of relaxant potency in dependence on antagonistic stimuli tracheal relaxation by the beta-2 sympathomimetics (+/-)-salbutamol (+/-)-fenoterol, and (+/-)-formoterol was compared to (-)-isoprenaline in guinea pig tracheae partially and maximally precontracted by carbachol. In partially precontracted tracheae, salbutamol, fenoterol and formoterol exerted maximum relaxation with low EC50 of 20, 5.6 and 0.29 nmol/l, respectively. In maximally precontracted tracheae, however, salbutamol, fenoterol and formoterol were only partial agonists for relaxation with different intrinsic activities (0.62, 0.62 and 0.77, respectively) and increased EC50 (120, 50 and 3.6 nmol/l, respectively). A reduction of relaxant potency by increased muscarinic stimuli was also observed for beta-1 adrenoceptors stimulated by (-)-noradrenaline after blockade of beta-2 adrenoceptors. In order to investigate if the reduced relaxant potency of beta-2 sympathomimetics was caused by a reduced spare receptor capacity or a reduced intrinsic activity for stimulation of adenylate cyclase (AC), we performed experiments in membranes from lung and tracheal cells. In radioligand binding, beta-2 sympathomimetics recognized the high-affinity state (57%) of the beta-2 adrenoceptor with a lower effectiveness than (-)-isoprenaline, which exhibited a 100-fold higher affinity for high over low-affinity states. Dissociation constants for the low-affinity state matched EC50 for AC stimulation. Intrinsic activities (%) for AC stimulation were significantly lower for salbutamol (67%), fenoterol (67%) and formoterol (89%) than for (-)-isoprenaline (100%), indicating that the reduced relaxation potency of the beta-2 sympathomimetics of maximally precontracted tracheae is caused by a reduced intrinsic activity for AC stimulation. It might be speculated that formoterol could improve drug therapy of asthma due to its high binding affinity and its high intrinsic activity for relaxation.

Adenylyl Cyclases↗
PubMed2003

Use of a subcutaneous beta-sympathomimetic pump for the treatment of fetal congenital complete heart block. A case report.

BACKGROUND: Complete heart block is the most common congenital heart block diagnosed in the fetalneonatal period. Maternal administration of beta-sympathomimetic agents has been used to treat this condition in the fetus. We know of no previous reports of the delivery of beta-sympathomimetics via a continuous subcutaneous pump for management of this condition. CASE: An intrauterine gestation at 28 5/7 weeks complicated by fetal congenital complete heart block was successfully managed to term with maternal administration of a beta-sympathomimetic agent via a continuous subcutaneous pump. CONCLUSION: Maternal administration of beta-sympathomimetic agents by a continuous subcutaneous pump in cases of fetal congenital complete heart block may help prolong pregnancy by preventing hydrops fetalis and avoiding confounding problems of prematurity. However, it should be used with caution due to the potential for dilated cardiomyopathy in the infant.

Adult↗
PubMed1990

L-tyrosine potentiates the anorexia induced by mixed-acting sympathomimetic drugs in hyperphagic rats.

The effects of L-tyrosine (L-TYR) on the anorectic activity of several mixed-acting sympathomimetics were determined during the dark cycle in rats made hyperphagic by food deprivation. L-TYR (200 mg/kg) significantly potentiated the anorectic activity of phenylpropanolamine, (-)-ephedrine and (+)-amphetamine by 48, 50 and 37%, respectively. When the dose of L-TYR was varied (25-400 mg/kg), a significant dose-dependent relationship was noted. The observed potentiation was positively correlated with increases in brain TYR concentrations; blockade of L-TYR uptake into the brain by the coadministration of L-valine prevented this potentiation. Various other L-amino acids, as well as D-TYR, failed to mimic the potentiating action of L-TYR. As determined by alpha-methyl-p-TYR pretreatment, the L-TYR-induced potentiation was dependent upon increased catecholamine synthesis. Although various other mixed-acting sympathomimetic anorexiants were similarly potentiated by L-TYR, the direct-acting beta-2 adrenoceptor anorexiants, salbutamol and methoxyphenamine, were not. These results indicate that L-TYR specifically potentiates the anorectic activity of the studied mixed-acting sympathomimetics and are consistent with the requirement of the central conversion of L-TYR to catecholamines via TYR hydroxylase for this response. The possibility that the effect of mixed-acting sympathomimetics is normally limited by the availability of L-TYR is suggested.

Amino Acids↗
PubMed1988

[Possibilities and limitations of using inhaled sympathomimetics in patients with bronchial asthma in older age groups].

Using a method of circadian ECG monitoring, the authors detected a peculiar phenomenon of frequent arrhythmic action of sympathomimetic inhalants in patients with bronchial asthma, mainly during remission. Possible interpretation of the results obtained was as follows: reduction during remission of functional beta block including heart block determining "cardioprotective" action in sympathomimetic inhalations; depletion of reserves of myocardial sympathetic mediators at the height of exacerbation of bronchial asthma; peculiarities of absorption of sympathomimetic inhalants with relation to a stage of disease. The authors discussed the potentialities and limitations of the use of sympathomimetic inhalants during exacerbation and remission of bronchial asthma with relation to patients' age and concomitant coronary heart disease.

Administration, Inhalation↗
PubMedDate not supplied

[Sympathomimetic drugs in the newborn infant].

In newborn infants with compromised clinical conditions, it is frequently necessary to improve the perfusion of the vital organs, and the choice often falls on sympathomimetic drugs. However their appropriate use is still discussed and the difference of the opinions about their choice is partially due to scarcity of controlled clinical studies. The purpose of this study is to supply, on the basis of the present knowledges, the opportunity of a rational choice and use of the sympathomimetic drugs in the neonate. The Authors consider the development of the cardiovascular sympathetic innervation and the different responsiveness to sympathomimetic drugs of the human foetus, compared to those of the animal foetuses. Then they discuss the pharmacological characteristics of some of the most important sympathomimetic drugs: adrenaline, isoproterenol, dopamine, dobutamine, indicating choice, and clinical use of them.

Autonomic Nervous System↗
PubMed1983

Effect of outpatient treatment of asthma with beta agonists on the response to sympathomimetics in an emergency room.

It has been suggested that tolerance to the bronchodilating effects of sympathomimetics may develop in asthmatic patients after long-term use of these agents. In an emergency room setting, the effects of inhaled and injected sympathomimetic therapy in 58 patients who had pretreated themselves with beta agonists were compared with the results observed in 38 patients who had not used such drugs. The two groups had similar degrees of obstruction on presentation and were also well-matched with respect to the clinical features of their illness. Both populations showed equal responses to treatment; no significant differences were found in either the amount of bronchodilation or the incidence of adverse effects in those who had or had not taken sympathomimetics as outpatients. These findings indicate that drug resistance does not account for outpatient treatment failures with sympathomimetics and that beta agonists can be usefully employed in the treatment of acute asthma, irrespective of a patient's medication history.

Adolescent↗
PubMed1983

Intrinsic sympathomimetic activity of pindolol. Evidence for interaction with pretreatment sympathetic tone.

Eighty-six hypertensive patients were treated with pindolol, a beta-adrenergic blocking drug with intrinsic sympathomimetic activity. To evaluate the interactions between beta-blockade, intrinsic sympathomimetic activity, and the level of pretreatment sympathetic activity, blood pressure, heart rate, and forced expiratory volume in one second (FEV1) were examined before and during a 15-week treatment program. The response of patients with a relatively higher pretreatment sympathetic tone reflected by a resting heart rate equal to or greater than 80 beats per minute (Group I) was compared with the response of patients with a lower pretreatment heart rate (less than 80 beats per minute) (Group II). Decreases in mean blood pressure were similar in the two groups. In patients in Group I, the net effect of pindolol was a modest decrease in heart rate and FEV1, supporting the concept that when sympathetic tone is relatively high, the beta-blocking effect is dominant. In contrast, patients in Group II showed little change in heart rate or FEV1 during pindolol treatment, reflecting a balance between the intrinsic sympathomimetic activity and beta-blocking effects of pindolol. Thus, the intrinsic sympathomimetic activity of pindolol is physiologically evident, and relative impact is dependent on the pretreatment level of sympathetic tone.

Clinical Trials as Topic↗
PubMedDate not supplied

Pharmacokinetics of non-prescription sympathomimetic agents.

The pharmacokinetics of non-prescription sympathomimetic agents are discussed with respect to absorption from the gastrointestinal tract, volumes of distribution, metabolism and renal excretion. Where specific data are not available, postulations are made with inference from the chemical structures of these agents, or from studies with other drugs. No studies on hypertensive patients have been found, but attempts are made to correlate any possible changes in the pharmacokinetics of these sympathomimetic agents to hypertensive patients as a high proportion of the elderly population is hypertensive. Sympathomimetic agents with lesser polar hydroxyl groups, for example, are thought to be more lipophilic and are more readily absorbed from the gastrointestinal tract, have higher volumes of distribution, and are more extensively metabolized. Major metabolic pathways include oxidation, deamination, demethylation, and conjugation. Most of these agents are excreted primarily through the kidneys and due to their basic nature, the rate of excretion is dependent on urinary pHs. Any alteration in kidney functions such as in the aged is, therefore, expected to have some clinical significance on the pharmacokinetics of these agents.

Age Factors↗
PubMed1998

Do parasympatholytic effects of long-acting beta 2-sympathomimetics contribute to their relaxant effects in airway smooth muscle cells?

To address the hypothesis of whether functional antagonistic effects of long-acting beta 2-sympathomimetics (formoterol and salmeterol) might be supported by direct antagonistic effects on muscarinic acetylcholine receptors (mAChR), we performed radioligand binding experiments with 3H-quinuclidinyl-benzilate in membranes of airway smooth muscle cells (calf tracheal myocytes). beta 2-Sympathomimetics (short- and long-acting) were compared to catechol-ethanolamines and catechol-ethylamines. Tracheal myocytes were characterized by a high density of mAChR 1017 +/- 17 fmol/mg, which exceeds that of beta 2-adrenoceptors 20-fold. The affinities of drugs were determined by competition binding. Dissociation constants ¿pKD-values) of formoterol (5.04 +/- 0.05) and salmeterol (5.24 +/- 0.04) matched that of ACh (5.37 +/- 0.03) and were significantly higher than that of the mAChR-agonist carbachol (4.65 +/- 0.03). pKD-values of mAChR-agonists were strictly dependent on GTP-concentration (> 50-fold difference between high- and low-affinity states), in contrast to those of formoterol, thereby characterizing formoterol as an mAChR-antagonist. A 10-fold lower affinity of the related compound fenoterol (3.94 +/- 0.02) hinted at the formyl-amino moiety of formoterol as a structural determinant of high-affinity whereas a 100-fold lower affinity of salbutamol as compared to salmeterol suggested the aliphatic side chain was a structural determinant of high affinity. The high affinity of dobutamine (4.96 +/- 0.02) and dopexamine (6.20 +/- 0.02) provided evidence that high affinity can be found not only for catechol-ethanolamines with long side chains but also for catechol-ethylamines. The question of whether high local concentrations after inhalation of long-acting beta 2-sympathomimetics could contribute to their therapeutical effects by antagonism with ACh on mAChR remains to be answered.

Adrenergic beta-Agonists↗
PubMed1982

Sympathomimetic effects of amezinium on the cardiovascular system and plasma catecholamines in man.

The cardiovascular effects of the sympathomimetic agent amezinium were investigated in a double-blind, placebo-controlled, randomized trial in six volunteers. Before and 2 h after oral administration of amezinium 30 mg or placebo the cardiovascular responses to orthostatic stress, induced by 80 degrees passive head-up tilt, were assessed by recording blood pressure, systolic time intervals, and echocardiogram. Plasma catecholamines were also determined. After amezinium treatment, the average supine systolic blood pressure was increased by +30 mm Hg and after tilting it remained above both the pre-treatment and placebo values. Compared to placebo, amezinium elicited only minor changes in heart rate and diastolic blood pressure. The effect of amezinium on the pre-ejection period corrected for heart rate (PEPc) and mean velocity of fiber shortening (VCFmean) indicated positive inotropic properties. Its effects were distinctly more pronounced during tilt than with the subjects supine. Plasma concentrations of noradrenaline and adrenaline were not influenced by amezinium during rest or tilt. From these results and previous research it is concluded that amezinium induces its sympathomimetic effects by preferentially inhibiting the re-uptake of noradrenaline which is released by the drug itself, or by sympathetic activation during tilt. This mechanism of action might explain the pronounced sympathomimetic effects of the drug, especially during orthostatic stress.

Adult↗
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↗
PubMed1991

Outcome of very-low-birth-weight infants exposed to beta-sympathomimetics in utero.

In this study we examined neonatal and early childhood outcomes after intrauterine exposure to beta-sympathomimetic agents on infants with birth weights less than or equal to 1500 gm. The hospital courses and anthropomorphic, developmental, and neurologic development of 201 infants exposed to one or more beta-sympathomimetic agents (isoxsuprine, 33; ritodrine, 70; terbutaline, 43; combination, 55) were analyzed and compared with those of 130 control infants of similar birth weight. One hundred and seventy-seven infants had follow-up to 1 year of age, 101 to age 3, and 58 to age 4. When treatments consisting of a single beta-sympathomimetic or no treatment were compared, there were no statistically significant overall differences found in growth and development or in most of the short-term measures of infant well-being. However, significant overall differences with no evidence of confounding by time-related effects were found for the following; mortality, none greater than terbutaline; maximum positive inspiratory pressure when respiratory distress syndrome was present, none greater than terbutaline; neonatal trauma, terbutaline greater than ritodrine. Other differences were found in conjunction with evidence of time-related confounding, or within specific time intervals. It should be noted that these differences are not necessarily due to effects of the different treatments, as the data are observational.

Female↗
PubMed1987

Sympathomimetics and exercise enhancement: all in the mind?

During the 1972 Olympic Games, a 16 year old American athlete was compelled to return a gold medal and was disqualified from further participation. Rick Demont had used a sympathomimetic drug (ephedrine) prior to competition for treatment of his asthma as prescribed by his physician. The present research was carried out to investigate whether the administration of a sympathomimetic drug enhances maximal performance in the normal healthy individual in terms of physiological and psychological processes? Ten subjects participated in a double-blind, cross-over, counterbalanced incremental cycle ergometer test on two different occasions, once after ingesting placebo, once after ingesting ephedrine. Repeated measures ANOVA's revealed no significant differences in any of the cardiopulmonary (VE, VO2, VCO2, RQ and AT), cardiovascular (HR, BP, O2 Pulse, RPP) and psychophysiological (RPE) variables between treatments. Findings in the current investigation suggest that no advantage is obtained with the use of sympathomimetic drugs to augment one's maximal aerobic capacity.

Blood Pressure↗
PubMed1991

L-tyrosine fails to potentiate several peripheral actions of the sympathomimetics.

We have recently reported the ability of L-tyrosine (L-TYR) to potentiate the anorectic activity of various mixed-acting sympathomimetics including phenylpropanolamine (PPA), l-ephedrine (EPH) and d-amphetamine (AMP). Included in those studies was the attenuation of L-TYR's effect when coadministered with L-valine, a large neutral amino acid which competes with L-TYR for uptake into the brain, suggesting a central locus for the action of L-TYR. To determine to what extent L-TYR can potentiate peripheral actions, we investigated the effects of L-TYR with either PPA (20 mg/kg), EPH (20 mg/kg) or AMP (1.75 mg/kg) on gastric transit, gastric retention and intrascapular brown adipose tissue thermogenesis. In each of the paradigms studied, PPA, EPH and AMP significantly increased the expected sympathomimetic-mediated response, but no potentiation of L-TYR was observed. These results are consistent with the hypothesis that L-TYR potentiates the anorectic activity of the mixed-acting sympathomimetics largely via an action at a central locus.

Adipose Tissue, Brown↗
PubMed2003

Central serous chorioretinopathy associated with administration of sympathomimetic agents.

PURPOSE: To report central serous chorioretinopathy associated with excessive use of compounds with sympathomimetic activity. DESIGN: Observational case series. METHODS: Four patients presented with clinical and fluorescein angiographic evidence of central serous chorioretinopathy. All patients expressed a concomitant psychogenic stress and high-dose ingestion of pseudoephedrine, oxymetazoline, or 3,4-methylenedioxymethamphetamine, all of which possess sympathomimetic properties. RESULTS: In all cases, resolution of central serous chorioretinopathy coincided with cessation of the medication. CONCLUSIONS: Patients afflicted with central serous chorioretinopathy should be notified about its possible association with sympathomimetic medications.

Adult↗
PubMed1999

Changes in renal blood flow in response to sympathomimetics in the rat transplanted and denervated kidney.

BACKGROUND: Renal denervation and re-innervation may affect vascular responses to sympathomimetics, which may play a role in the maintainance of renal blood flow (RBF) following renal transplantation. The purpose of the present study was to elucidate pharmacological alteration of the renal sympathetic response following kidney transplantation. Using the rat kidney transplantation model, we focused on responses to various sympathomimetics in order to investigate the effects of sympathetic denervation and functional remodulation mechanisms in the transplanted kidney. METHODS: Male isogenic rats underwent unilateral kidney denervation or kidney transplantation accompanied by unilateral native nephrectomy. Renal blood flow was evaluated using a laser Doppler flow meter following bolus injection of 50 microg/kg dopamine and continuous infusion of 60 microg/min phenylephrine (PE) at 0, 30, 60, 90 and 240 days after transplantation as well as at 30 days after denervation. RESULTS: Bolus injection of dopamine (50 microg/kg) induced an initial reduction in RBF (that of alpha-adrenoceptors) followed by a long-lasting increase in RBF (that of beta-adrenoceptors) in the native kidney. In grafted or denervated kidneys, the dopamine-induced decrease in RBF mediated by alpha-adrenoceptors was markedly enhanced while the increase in RBF mediated by an action of dopamine on beta-adrenoceptors was blunted. The effects of the post-transplant period on vascular responses to dopamine were significant, but not completely synchronized with the native kidney, even at 240 days. Continuous infusion of PE (60 microg/min) produced a gradual increase in RBF in the native kidney, whereas a sudden reduction (i.e. breakthrough in autoregulation) was observed in the denervated and transplanted kidney. CONCLUSIONS: The responses to sympathomimetics in the grafted kidney were shifted towards flow reduction (i.e. enhanced vasoconstriction via stimulation of alpha-adrenoceptors and blunted vasodilatation via stimulation of beta-adrenoceptors. This functional impairment was recovered in a time-dependent manner. In addition, the hemodynamic autoregulation system in the kidney deteriorated following transplantation or denervation.

Animals↗