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PubMed2002

Informed decision-making on sympathomimetic use in sport and health.

The International Olympic Committee, the World Anti-Doping Agency, and International Sport Federations have banned and restricted the use of many stimulants including prescription and over-the-counter medications and dietary supplements. In addition to elite athletes, people of all ages use stimulants in attempts to improve athletic performance, alter body composition, and increase levels of energy. Here we introduce a seven-stage model designed to facilitate informed decision-making by individuals taking or thinking of taking stimulants for sport, health, and/or appearance reasons. We review for amphetamines, over-the counter sympathomimetics, and caffeine their performance-enhancing and performance-degrading effects, health benefits and mechanisms of action, medical side effects, and legal, ethical, safety, and financial implications.

Amphetamines↗
PubMed1982

Beta-adrenoceptor blockade and atrio-ventricular conduction in dogs. Role of intrinsic sympathomimetic activity.

1 Atrio-ventricular conduction and its modifications induced by six beta-adrenoceptor blocking agents and isoprenaline have been investigated in the anaesthetized dog using the extrastimulus technique and measuring atrial (AERP), nodal (NERP), global (GERP) effective refractory periods as well as global functional refractory period (GFRP). 2 When beta-adrenoceptor blockade was produced by (+/-)-propranolol (beta 1 + beta 2-adrenoceptor blockade) which is devoid of intrinsic sympathomimetic activity (ISA) but has membrane stabilizing effects (MSE), sotalol (beta 1 + beta 2-adrenoceptor blockade, no ISA, no MSE) and atenolol (beta 1-adrenoceptor blockade, no ISA, no MSE), all parameters were significantly increased. When beta-adrenoceptor blockade was achieved with pindolol (beta 1 + beta 2-adrenoceptor blockade) and practolol (beta 1-adrenoceptor blockade) which have ISA but no MSE, all parameters remained unchanged, as was also the case with (+)-propranolol, which has MSE but neither ISA nor beta-adrenolytic properties. 3 Isoprenaline at high doses significantly reduced the refractory periods but when infusion was stopped, marked but reversible conduction depression was observed. 4 It thus appears that beta-adrenoceptor blockade but not MSE is responsible for the onset of atrial and AV-conduction impairment and that ISA affords protection against this impairment.

Adrenergic beta-Antagonists↗
PubMed1982

Intrinsic sympathomimetic activity and coronary blood flow.

1 The effects of four beta-adrenoceptor blocking agents, propranolol, pindolol, practolol and atenolol, used in doses inducing the same degree of beta 1-adrenoceptor blockade, have been investigated on regional myocardial blood flow (microspheres) and coronary vascular resistance in the normal and ischaemic myocardium of the anaesthetized dog. 2 In the ischaemic and non-ischaemic myocardial areas, transmural blood flow was significantly reduced by propranolol and atenolol which are devoid of intrinsic sympathomimetic activity (ISA) while it remained unaffected by beta-adrenoceptor blocking drugs endowed with ISA, whether cardioselective (practolol) or not (pindolol). In non-ischaemic areas, only propranolol and atenolol increased coronary vascular resistance. 3 Regarding coronary blood flow distribution between the epicardium and endocardium, only propranolol and pindolol induced a favourable redistribution towards the endocardium increasing the endo/epi flow ratio, while practolol and atenolol were ineffective. 4 These results suggest that ISA is of major importance in maintaining coronary flow especially in the ischaemic myocardium but that it is not involved in the mechanisms underlying coronary blood flow redistribution between the different myocardial layers.

Adrenergic beta-Antagonists↗
PubMed1982

The effect of intrinsic sympathomimetic activity of beta-adrenoceptor blockers on circadian heart rate.

1 The effect of a beta-adrenoceptor blocker without intrinsic sympathomimetic activity (propranolol) and a beta-adrenoceptor blocker with ISA (pindolol) on circadian heart rate was studied in 10 patients (3 women and 7 men) with an average age of 55 years and the following diagnoses: coronary heart disease (n = 7) and hypertension (n = 3). The therapy was carried out in a randomized, cross-over study, with 3 x 40 mg propranolol and 3 x 5 mg pindolol. 2 Propranolol lowered the averaged circadian heart rate significantly (P less than 0.001) from 78 to 68 beats/min. The rate decreased both during the day and at night and the reduction was greater the higher the control value. The minimal hourly heart rate also decreased significantly (P less than 0.005) from 65 to 69 beats/min. 3 After pindolol the averaged circadian heart rate was not markedly changed. It reached a stable rate of around 70 beats/min. At a heart rate of below 70 beats/min an increase in rate was observed, whereas above 70 beats/min a reduction was found. The mean heart rate during the day remained unchanged. There was a significant relationship between the level of the control heart rate and the decrease in rate (r = 0.85, P less than 0.005). 4 In a bicycle exercise test of 1 Watt/kg body weight over a period of 6 min, both beta-adrenoceptor blockers lowered blood pressure and heart rate to the same extent.

Adrenergic beta-Antagonists↗
PubMed1982

The influence of beta-adrenoceptor blocking drugs with and without intrinsic sympathomimetic activity on the hormonal responses to hypo- and hyperglycaemia.

1 The effects of oral doses of pindolol (15 mg), metoprolol (200 mg) and propranolol (160 mg) on the response to insulin-induced hypoglycaemia and an oral glucose load were investigated. 2 Serum insulin and serum C-peptide secretion in response to a glucose load were inhibited (2P less than 0.01) by metoprolol and propranolol but not by pindolol. 3 During hypoglycaemia metoprolol and propranolol inhibited the clearance of insulin (2P less than 0.01) and caused a delay of glucose nadirs. 4 Adrenaline secretion during hypoglycaemia was markedly increased by metoprolol and propranolol but not by pindolol. 5 The counterregulatory response of growth hormone, ACTH and cortisol was increased following metoprolol and propranolol but not after pindolol. 6 The hypoglycaemic symptoms and signs showed a prevalence of sweating and prolonged changes in skin conductivity whereas palpitations were not observed during beta-adrenoceptor blockade. Asymptomatic hypoglycaemia did not occur. 7 The absence of unphysiological rises in adrenaline, growth hormone, ACTH and cortisol supports the use of a beta-adrenoceptor blocker with intrinsic sympathomimetic activity.

Adrenergic beta-Antagonists↗
PubMed1987

Cardiac effects of beta-adrenoceptor blockade with intrinsic sympathomimetic activity during submaximal exercise.

1. beta-adrenoceptor blocking agents with intrinsic sympathomimetic activity (ISA) are characterized by lesser depression of cardiac performance during low levels of sympathetic stimulation than beta-adrenoceptor blocking agents lacking ISA. Studies of the effects of ISA on cardiac output and on the determinants of myocardial oxygen demand during submaximal exercise are described and distinct differences between beta-adrenoceptor antagonists with and without ISA emerge. 2. At doses which produce similar effects on maximal exercise heart rate, and resting and exercise systolic blood pressure, pindolol, a beta-adrenoceptor blocking agent with substantial ISA, allows a higher submaximal exercise cardiac output and submaximal heart rate X systolic blood pressure product than does propranolol, a beta-adrenoceptor antagonist without ISA. 3. These findings may have clinical relevance in specific groups of patients such as those with arterial hypertension, where the preservation of cardiac function may allow for a more physiologic exercise response. Implications in patients with coronary artery disease and chronic heart failure await further study.

Adrenergic beta-Antagonists↗
PubMed1987

Large arteries in hypertension: heterogeneous haemodynamic response to beta-adrenoceptor antagonists with and without intrinsic sympathomimetic activity.

1. Hypertension is associated with a distension of the large arteries and consequently a marked reduction in arterial compliance, which does not result merely from the mechanical effects of elevated arterial pressure but also from early functional and/or structural changes in the arterial walls. This suggests that one of the aims of antihypertensive therapy should be to reverse these arterial abnormalities in the hope of protecting the patient from the atherosclerotic complications of hypertension. 2. Studies have been carried out to compare the effects of equieffective antihypertensive doses of pindolol and propranolol on the arterial circulation in patients suffering from essential hypertension. After 3 months therapy pindolol produced a dilatation of the brachial artery with an increase in arterial compliance and blood flow. In contrast, propranolol, despite comparable antihypertensive effects, did not influence brachial artery circulation. 3. These different effects on the arterial circulation presumably reflect the differing pharmacological properties of the two beta-adrenoceptor antagonists and suggest that the intrinsic sympathomimetic activity of pindolol may be responsible for the qualitative differences in the arterial responses to the two drugs. 4. The results reviewed here reveal that even when two drugs of the same class are used to treat patients with essential hypertension the effects of these agents on arterial haemodynamics can vary greatly and are unrelated to the degree of blood pressure lowering. Thus, pindolol, in contrast to propranolol, not only lowers blood pressure but also reverses some of the changes in arterial haemodynamics which are characteristic of hypertensive disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

The beta-adrenoceptor antagonist carteolol and its metabolite 8-hydroxycarteolol have different intrinsic sympathomimetic activities.

We have tested the effects of carteolol and 8-hydroxycarteolol on cAMP generation in S49 lymphoma and BC3H1 smooth muscle-like cells. Carteolol was a high affinity beta-adrenoceptor antagonist in both systems but did not stimulate cAMP accumulation. The metabolite 8-hydroxycarteolol also was a high affinity antagonist. In contrast to its parent compound, however, it possessed an agonistic component which was considerably stronger than that of other beta-adrenoceptor blockers with intrinsic sympathomimetic activity, e.g. dichloroisoprenaline, pindolol, or celiprolol. These results suggest that metabolites can possess different pharmacodynamic properties in terms of beta-adrenoceptor interaction relative to parent compounds.

Carteolol↗
PubMed1995

Effects of glucocorticoids and sympathomimetic agents on basal and insulin-stimulated glucose metabolism.

The mechanisms responsible for glucocorticoid-induced insulin resistance remain unclear. Glucocorticoids show several interactions with the sympatho-adrenal system which may contribute to this decrease in insulin sensitivity: they enhance the synthesis and actions of catecholamines, but abolish insulin-induced activation of muscle sympathetic nerve activity. The present study was performed in order to investigate the effects of the interactions between glucocorticoids and the sympatho-adrenal system on insulin sensitivity. Basal and insulin-stimulated glucose metabolism was measured in healthy human subjects during four 2-h clamp studies as follows: control (C); after taking oral dexamethasone (2 mg daily) for 2 days (D); after taking oral ephedrine sulphate (40 mg daily) for 2 days (E); and after taking dexamethasone+ephedrine (D+E). Glucose uptake, production and oxidation were calculated from plasma 13C glucose and exhaled 13CO2 during constant tracer infusion of U-13C glucose. Basal glucose production, utilization and oxidation were similar in all four studies. During hyperinsulinaemia, glucose uptake was reduced by 51.5% with treatment D, by 25.9% with treatment E, and by 49.6% with D+E. Glucose oxidation was reduced by 54.0% with treatment D, by 24.0% with treatment E, and by 57.2% with D+E. Hepatic glucose production was completely suppressed in all four studies. It is concluded that both dexamethasone and ephedrine decrease insulin-mediated glucose uptake and oxidation. Co-administration of ephedrine does not suppress the glucocorticoid-induced alterations of glucose metabolism. This indicates that glucocorticoid-induced insulin resistance is not related to the inhibition of muscle sympathetic nerve activity. These results suggest instead that glucocorticoids and sympathomimetic agents may impair glucose metabolism by common actions.

Adult↗
PubMed1958

The action of sympathomimetic amines on heart rate in relation to the effect of reserpine.

When the heart-lung preparation is made from a dog treated with reserpine, catechol amines such as noradrenaline and isoprenaline have a greater effect on the rate of the heart than they have in a preparation from a normal dog. Other sympathomimetic amines such as tyramine and ephedrine, on the other hand, are found to have lost their action. Since treatment with reserpine has been shown to cause the store of noradrenaline in the heart to disappear, and the infusion of noradrenaline into the preparation made from a reserpine-treated animal restores the action of tyramine, it is concluded that substances like tyramine and ephedrine normally act by liberating noradrenaline from the store, and do not act directly. Cocaine, like reserpine, increases the effect of noradrenaline and decreases the effect of tyramine on the heart rate; it appears to block the release of noradrenaline from the store in the heart.

Amines↗
PubMed1959

A hypothesis concerning the effect of cocaine on the action of sympathomimetic amines.

There is a store, perhaps in chromaffin tissue, of noradrenaline in tissues with a sympathetic innervation. The store is depleted by treatment with reserpine. Sympathomimetic amines like tyramine act only when this store is present and have no effect when the store is depleted. They also fail to act in the presence of cocaine. Catecholamines like noradrenaline have a much greater action than usual when the store is depleted, and they have a much greater action in the presence of cocaine. It is suggested that cocaine has the effect of blocking release from the store, so that the action of tyramine is abolished and the spontaneous release from the store which is responsible for the normal (low) sensitivity to noradrenaline is stopped. Noradrenaline is taken up into the store in the heart and the vessel wall from the blood, and the disappearance of noradrenaline from the blood is in part due to this uptake and not entirely to destruction. Cocaine may prevent this uptake of noradrenaline by the tissue stores. Experiments on rabbit atria, on the vessels of the rabbit ear and on the heart-lung preparation are described which are consistent with this hypothesis.

Animals↗
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↗
PubMed1961

Interactions of sympathomimetic drugs and their antagonists on the isolated atrium.

In the isolated guinea-pig atrium, phenoxybenzamine and other antagonists of sympathomimetic drugs and the adrenergic nerve blocking agent guanethidine inhibited the action of butyrylcholine and tyramine and potentiated the action of noradrenaline. Also in the isolated guinea-pig atrium, phenoxybenzamine and cocaine abolished the parasympathetic, and potentiated the sympathetic, effects of vagus stimulation.

Choline↗
PubMed1962

Response of normal, denervated, and reserpine-treated arteries to sympathomimetic amines and nicotine in dogs.

The sensitivity of normal, denervated carotid arterial segments, and of carotid arteries of dogs previously treated with reserpine, to sympathomimetic amines and nicotine has been compared using isolated perfused segments of these vessels. Arteries from animals and arterial segments treated with reserpine, denervated by peri-arterial stripping or by re-anastomosing of segments removed and reversed, both showed an increased sensitivity to noradrenaline which correlated well with a decrease in tissue noradrenaline content. Tyramine did not produce vasoconstriction in denervated vessels, but some constriction was observed when the vessels had been pretreated with noradrenaline or with dopamine or dopa. The effect of nicotine upon dog carotid arterial segments was recorded 130 times. The most frequent response was vasodilatation. This involved both the arterial wall per se and the vasa vasorum. The vasodilatation in response to nicotine was seen in arteries from normal and reserpine-treated animals and in denervated vessels.

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↗
PubMed1968

Action of various sympathomimetic amines on the isolated stripped vas deferens of the guinea-pig.

1. The contractile potencies of some sympathomimetic amines and cholinergic drugs were studied in the isolated, stripped vas deferens of the guinea-pig.2. alpha-Methylnoradrenaline, adrenaline and metaraminol produced the same relative maximal responses as noradrenaline, which served as reference drug; on the other hand, octopamine, dopamine and alpha-methyldopamine were much less active. Short term pretreatment of the animals with reserpine did not affect the maximal relative responses.3. Tyramine, alpha-methyl-m-tyramine and hordenine methiodide had little effect on the untreated preparation. In the presence of just threshold concentrations of noradrenaline, the relative maximal responses to tyramine and hordenine methiodide were markedly increased.4. The relative maximal response to carbachol was the same as that to noradrenaline, while that to DMPP was smaller. In contrast to carbachol, the action of DMPP was potentiated by pretreatment of the preparation with noradrenaline.

Animals↗
PubMed1969

Steroid potentiation of responses to sympathomimetic amines in aortic strips.

1. Responses to catecholamines (adrenaline, noradrenaline, nordefrine) were enhanced by 17beta-oestradiol, progesterone and desoxycorticosterone in untreated and reserpine pretreated aortic strips. Responses to tyramine, believed mediated via endogenous catecholamines, were enhanced only in untreated strips.2. Responses to sympathomimetic amines lacking the catechol nucleus (phenylephrine, synephrine, methoxamine) were potentiated inconsistently by the steroids and reserpine pretreatment reduced markedly the frequency of potentiated responses.3. Known inhibitors of catechol-O-methyl transferase (tropolone, U-0521, pyrogallol) potentiated responses to catecholamines and abolished the enhancing effects of the steroids-when the steroids were given first, there was no further increase in response to catecholamines on adding inhibitors of catechol-O-methyl transferase.4. Experiments with the oil-immersion technique, to eliminate diffusion of drug from the tissue, indicated that 17beta-oestradiol, progesterone and desoxycorticosterone decreased the rate at which aortic strips inactivated adrenaline by O-methylation.5. It is concluded that 17beta-oestradiol, progesterone and desoxycorticosterone potentiate responses to catecholamines in aortic strips by inhibiting a major mechanism for their inactivation.

Animals↗
PubMed1969

Effects of reserpine on the disposition of sympathomimetic amines in vascular tissue.

1. The effects of reserpine pretreatment on the intrinsic inactivation of low concentrations of phenylephrine and noradrenaline in strips of rabbit thoracic aorta were assessed by measuring the rates of relaxation, after oil immersion to prevent loss of active amine by diffusion into the surrounding medium.2. Reserpine pretreatment considerably augmented the amplitude of responses to low concentrations of phenylephrine, noradrenaline and nordefrine (Cobefrine).3. Reserpine pretreatment did not reduce the overall rate of inactivation of either phenylephrine or noradrenaline, but it did appear to decrease the contribution of uptake and storage, measured as an increased effect of enzyme inhibition and a decreased effect of cocaine on the rate of inactivation.4. The role of catechol-O-methyl transferase (COMT), but not that of monoamine oxidase (MAO), in terminating the action of noradrenaline was increased in strips from animals pretreated with reserpine. Thus it appears that interference with intraneuronal storage diverts active amine to inactivation by COMT in vascular tissue, rather than by MAO as has been previously suggested.5. As in preparations not treated with reserpine, inhibition of MAO alone had little effect on the rate of inactivation of noradrenaline, and this enzyme appears to function predominantly as an alternate pathway of little importance as long as COMT activity is unimpaired. Enzymatic processes accounted for about 85 and 70% of the inactivation of a low concentration of noradrenaline in reserpine pretreated and untreated preparations, respectively.6. Cocaine potentiated responses to noradrenaline and phenylephrine as effectively in reserpine pretreated as in untreated preparations, and inhibition of the pathways of enzymatic inactivation did not appreciably decrease the potentiation produced by this agent.7. The present results cannot be explained by the hypothesis that interference with amine inactivation by nerve uptake and storage is responsible for the potentiation of responses to noradrenaline or phenylephrine by either reserpine or cocaine, and emphasize the unrealiability of potentiation as an index of interference with mechanisms involved in terminating the action of sympathomimetic amines.

Animals↗