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At least 19 recordsLinked to original sources

PubMed1975

The influence of temperature increase, elevation of extracellular h+-concentration, and of triiodothyronine on the actions of phenylephrine, histamine, and beta-sympathomimetic drugs on rabbit aortic strips.

In the isolated preparation from the rabbit thoracic aorta, the affinities of the vasoconstrictor agents phenylephrine and histamine, as well as of the vasodilator beta-sympathomimetic drugs isoprenaline, fenoterol (TH 1165a), terbutaline, and salbutamol under the conditions of temperature increase, triiodothyronine and decrease of extracellular pH were investigated. It was observed that (1) a temperature increase from 25 degrees to 42 degrees C significantly indreased the maximal tension evoked by histamine, whereas that induced by the alpha-sympathomimetic drug phenylephrine was not altered significantly; the maximal relaxation caused by beta-sympathomimetic drugs either at 25 degrees or at 42 degrees C did not differ from one another; (2) the affinities of histamine, phenylephrine and of the beta-sympathomimetic drugs isoprenaline, fenoterol, terbutaline, and salbutamol each were comparable at either 25 degrees or 42 degrees C; the rank order of efficacy of the beta-sympathomimetic drugs is isoprenaline greater than fenoterol greater than salbutamol greater than terbutaline; (3) a decrease of the pH from 7.37 to 7.15 diminished the affinities of histamine and of the beta sympathomimetic drugs whereas that of the alpha-adrenergic drug phenylephrine was not altered. A further decrease of the pH to 6.8 diminished additionally the affinity of histamine and of isoprenaline, and especially that of the other beta-sympathomimetic drugs to such an extent that in the latter case complete dose-response curves could not be determined any more; (4) pretreatment of the animals with 0.4 mg/kg of triiodothyronine (T3) for two days, which strongly depressed the tension induced by either histamine or phenylephrine, did not alter the affinity of both drugs; T3 in vitro (10(-6) M) only diminished the affinity of histamine but left that of phenylephrine unaltered; pretreatment for two days with 0.2 mg/kg of T3 yielded a significant diminution of the pD2-values for two beta-sympathomimetic drugs investigated, namely isoprenaline and fenoterol; also the administration of T3 in vitro in a final concentration of 10(-6) M resulted in a diminution of the affinity of both beta-sympathomimetic drugs; (5) the results obtained show that also on the aorta beta-adrenoceptor stimulants are dependent on the metabolic state while alpha-adrenoceptor stimulants are not.

Adrenergic beta-Agonists↗

PubMedDate not supplied

A study of the relationship between cardiac beta-adrenoceptor blockade and intrinsic sympathomimetic activity in rats depleted of catecholamines.

1. The intrinsic sympathomimetic activity of a range of beta-adrenoceptor antagonists and its relationship to beta-adrenoceptor blockade was studied in pentobarbitone-anaesthetized, vagotomized rats which had been depleted of catecholamines by pretreatment with syrosingopine. Dichlorisoprenaline, practolol, oxprenolol, pindolol and acebutolol, produced dose-dependent positive chronotropic responses in this preparation. 2. The relationship between the dose requirements for this intrinsic sympathomimetic activity and beta-adrenoceptor-blocking activity was not the same for all drugs: (i) dichlorisoprenaline and practolol had intrinsic activity at all beta-adrenoceptor-blocking doses; and (ii) oxprenolol, pindolol and acebutolol had predominantly beta-adrenoceptor blockade at the lower dose levels and agonist activity only became significant at high doses relative to those producing beta-adrenoceptor blockade. 3. The positive chronotropic response to both practolol and pindolol was observed in rats which had been pithed and was antagonized by propranolol (0.1-3.0 mg/kg, i.v.), indicating that beta-adrenoceptors were involved. 4. It was concluded that the intrinsic sympathomimetic activity of beta-adrenoceptor antagonists was not a simple property as it was described by the relationship between the dose requirements for intrinsic sympathomimetic activity and for beta-adrenoceptor blockade as well as the degree of partial agonist activity.

Adrenergic beta-Antagonists↗

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↗

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↗

PubMed1978

[Use of sympathomimetics in the treatment of asthma].

There are many sympathomimetic products available in treatment of asthma, such as ephedrin, isoproterenol, orciprenalin, salbutamol, terbutalin..., used by oral or injectable route and spray. In the spray form, the sympathomimetic products have immediate and intense activity but the easiness of their use leads to a dose multiplication or overdose ineluctably, and thus involves cardiac and respiratory accidents which can be fatal. Their prescription should be slightly different according to the clinical type of asthma in the patient. On the other hand the oral sympathomimetic products are less inclined to overdose.

Albuterol↗

PubMed1976

Sympathomimetic-induced effects in the soleus muscle of the guinea-pig.

Sympathomimetic amines reduced the peak tension, time to peak and time to half-relaxation of indirectly elicited twitches of the guinea-pig soleus muscle in vivo. Clonic contractions of the soleus muscle were depressed by the amines. On a molar basis salbutamol and orciprenaline were 5.12 and 80.0 times less potent than (+/-)-isoprenaline in producing these effects. Results obtained with the beta-receptor antagonists propranolol, practolol and H35/25 suggest that the depression in skeletal muscle contractility is due to beta2-adrenoreceptor stimulation. The effects of the amines on twitches and clonic contractions of the guinea-pig soleus muscle are qualitatively similar to those reported previously in the cat soleus muscle preparation, which has been used to assess the possible tremorogenic actions of sympathomimetic bronchodilators. On a quantitative basis the molar dose-ratios of the sympathomimetics used, and the effects of beta-receptor antagonists on the responses, are similar in the two species.

Adrenergic beta-Agonists↗

PubMed1978

Uropharmacology: VIII. Sympathomimetic agents.

Sympathomimetic drugs stimulate the receptors of the sympathetic nervous system. Although the bladder possesses sympathetic receptors, sympathomimetic drugs, in general, have little effect on bladder function. Their most useful clinical applications on the urinary tract are to increase or decrease bladder resistance.

Animals↗

PubMed1977

The sympathomimetic activity of fenfluramine hydrochloride on rat vas deferens.

1. The peripheral, pharmacological effects of the anorexigenic agent, fenfluramine hydrochloride, have been investigated on rat isolated vas deferens. 2. Characteristic spiked contractions were observed within 2 to 3 min after exposure to fenfluramine; these contractions reached a rate of around 13 per min and were of variable height. 3. Pre-treatment of vasa with the indirectly acting sympathomimetic amine, tyramine, greatly reduced both the height and rate of contraction induced by fenfluramine. 4. The uptake inhibitor, desipramine, required a concentration in excess of 10 micronM to affect fenfluramine-induced contractions. Effects of desipramine on fenfluramine contractions were of equal magnitude whether desipramine was administered before fenfluramine or at the height of the fenfluramine-induced contractions. 5. Pre-treatment with debrisoquine (0.5 mM), reduced the contractions in response to fenfluramine over a period of time. 6. Fenfluramine, added to vasa from rats which had been injected intraperitoneally with 5 mg/kg reserpine 24 h and 48 h previously, failed to induce its characteristic contractions. 7. It is concluded that fenfluramine can be classed as an indirectly acting sympathomimetic amine on peripheral adrenergic nerve terminals.

Animals↗

PubMed1977

Metabolic actions of some sympathomimetic amines and their acetyl derivatives in the rabbit.

To study how acetylation affects the activity of sympathomimetic amines the effects of tyramine, amphetamine, ephedrine, phenylephrine, orciprenaline and salbutamol and of their O- and N-acetyl derivatives on blood glucose and free fatty acid concentrations were studied in the rabbit. Hyperglycemia was induced by all parent compounds except amphetamine which tended to have a weak hypoglycaemic action. Hyperlipaemia in the doses used was induced by ephedrine and orciprenaline but not by the other parent compounds. Usually acetylation decreased the metabolic effects of the compounds but O-acetylation of tyramine and salbutamol caused hyperlipaemia and O-acetylation of ephedrine increased its fatty acid-mobilizing action, perhaps as a consequence of increased lipid solubility of the compounds. The ultimate effects of the O-acetyl derivatives were probably at least partly due to deacetylation at their sites of action. However O-acetylation of sympathomimetics could perhaps be used to induce drug latentiation.

Acetylation↗

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↗

PubMed1977

Release of platelet 5-hydroxytryptamine by some anorexic and other sympathomimetics and their acetyl derivatives.

The effect on 5-hydroxytryptamine release from rabbit platelets to plasma of ten known sympathomimetic or anorectic phenethylamines and eight N- or O-acetyl derivatives of these substances were studied in order to find possible structure-action relationships and a possible correlation to the pulmonary hypertension inducing ability of some anorexigens. Among the mainly indirectly acting sympathomimetics amphetamine and ephedrine showed a similar high 5HT-releasing effect. Tyramine was slightly weaker, while the direct acting phenylephrine (metaoxedrine) and orciprenaline were much weaker. Acetylation increased the 5HT releasing effect of amphetamine, ephedrine and tyramine but decreased this effect of phenylephrine and orciprenaline. Among the anorectic phenethylamines the 5HT-releasing effect decreased in the following order, aminorex, amphetamine, clophorex, chlorphentermine, diethylpropion (amphepramon), phentermine. With regard to aminorex, which is a releaser of platelet 5HT and an inhibitor of both MAO activity and 5HT uptake in pulmonary tissue, it seems possible that the pulmonary hypertension can be caused by high concentration of free 5HT.

Animals↗

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↗

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↗

PubMed1975

Abnormal secretory response to parasympathomimetic and sympathomimetic stimulations from the submaxillary gland of rats treated with reserpine.

Rats treated with 0.5 mg/kg of reserpine per day for 7 days were anesthetized and submaxillary saliva was collected and analyzed for Na+, K+, Ca++ and protein concentrations. Salivary secretion was elicited by i.p. injections of carbamylcholine (50-100 mug/kg), phenylephrine (5 mg/kg) and isoproterenol (10 mg/rat). Saliva was also collected from untreated controls. Submaxillary glands were excised from both groups of animals at the termination of the secretory response, homogenized and analyzed. Glands from other animals were removed in the resting state and similarly processed. Pretreatment with reserpine resulted in decreased volumes of salvia and in elevated salivary concentrations of Ca++ and protein. Saliva from the reserpine-treated animals secreted in response to carbamylcholine had higher concentrations of Na+ and K+ than control saliva, particularly at the low rates of flow. Saliva secreted after stimulation with the two sympathomimetic secretagogues had lower concentrations of these two ions. Resting glands from the treated animals showed significant elevations in protein and Ca++ content and a significant decrease in K+ content. At the end of the secretory response to the three secretagogues, glands from treated animals showed a significantly higher Na+ content and a significantly lower K+ content than control glands. It is concluded that pretreatment with reserpine alters the secretory response of the rat submaxillary gland to both parasympathomimetic and sympathomimetic stimulation. This alteration results from a toxic lesion caused by reserpine in the salivary cells, which involves changes in their permeability to ions and in their energy resources. These in turn, result in an abnormal stimulus-secretion coupling mechanism. The possibility that the toxic lesion is related to alterations in Ca++ homeostasis is discussed.

Animals↗

PubMed1976

The adsorption of sympathomimetic agents by activated carbon hemoperfusion.

Sympathomimetic agents with mixed and pure alpha and beta adrenergic activity are adsorbed by coconut shell activated carbon from blood, sufficiently rapidly to markedly reduce the activity of these agents. The results of this study suggest that the site of injection of sympathomimetic agents being considered for correcting hypotension during activated carbon hemoperfusion be selected to permit systemic mixing before circulation into the adsorption device.

Adsorption↗

PubMed1979

[Investigations of the effect and mechanism of action of the beta-sympathomimetic ritodrine on the synthesis and release of dipalmitoyl-lecithin in the fetal rabbit lung (author's transl)].

For a period of 8 days, pregnant white New Zealand rabbits were treated either with the beta-sympathomimetic Ritodrine (1 mg/kg) body weight daily) or with 0.9% saline solution. The fetuses were delivered by caesarian section on the 25th and 30th day of gestation (term being 31 days). No significant difference was found between the Ritodrine and saline treated groups with respect to the levels of dipalmitoyl-lecithin (DPL) obtained from the homogenates as well as the alveolar lavages of the fetal lungs. These results indicate that with this experimental model, prepartum treatment with Ritodrine has no effect either on DPL synthesis or its release into the alveolar spaces. Furthermore, treatment with the beta-sympathomimetic produced no significant change in the concentrations of the specific glucocorticoid receptors in the cytosol and nuclei of the fetal lungs, and in addition, the lung cytosol glucose concentrations as well as the plasma corticosteroid levels were unaffected. These findings support the conclusion that the synthesis of DPL in the fetal lung is not stimulated by Ritodrine.

Animals↗

PubMed1979

Neonatal hypoglycemia after beta-sympathomimetic tocolytic therapy.

The effect of oral beta-sympathomimetic tocolytic therapy on neonatal serum glucose concentrations in the first several hours after delivery was examined in 12 babies. Hypoglycemia was noted in eight babies, and was sustained over at least a 30-minute period in five. The group with sustained hypoglycemia had a higher cord serum insulin concentration, a lower serum glucose nadir, and a more rapid initial rate of serum glucose disappearance than those babies with normoglycemia or transient hypoglycemia. Sustained hypoglycemia was observed in five of six babies delivered within two days of the termination of tocolytic therapy, but was not present in any of six babies delivered five or more days after the end of tocolytic therapy. Speculations as to the interaction between beta-sympathomimetic tocolytic drugs administered to the mother and fetal and neonatal glucose metabolism are made.

Ethanolamines↗

PubMed1978

Compartmental shift of potassium--a result of sympathomimetic overdose.

A 17-year-old youth was admitted with a serum potassium concentration of 1.8 mmol/l after taking an overdose of pseudoephedrine and choline theophyllinate. Apart from tachycardia, tachypnoea and ankle clonus, examination was normal as was the initial electrocardiograph. The hypokalaemia resolved, but there was an overall positive potassium balance of only 13 mmol. This suggests that the sympathomimetics provoked a compartmental shift of potassium perhaps indirectly by inducing hyperglycaemia and hyperinsulinaemia, as well as directly. Other factors known to affect body potassium distribution were excluded. The fact that features commonly associated with hypokalaemia could not be demonstrated may be explained by a normal body potassium content. Severe hypokalaemia caused by a compartmental shift occurs with large doses of sympathomimetics as well as in periodic paralysis.

Adolescent↗