Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal experiments were set up mainly to derive additional diagnostic data from the study of biochemical changes after acute head injury. In standardized experiments guinea pigs were subjected in groups of 20 to three identical head injuries, each of either 1.0 J or 1.5 J intensity. The trauma was likely to result in a concussion or contusion syndrome similar to that found in man; 40 animals served as controls. During the 60 min after injury observation and measurement of body functions did not reveal signs of a shock-like condition or hypoxaemia in the traumatized animals compared with control animals. Superficial anaesthesia probably did not influence the findings. Temperature and respiration were altered significantly in all the animals receiving head injuries. Blood gas analysis showed a decrease of standard bicarbonate only after the 1.5 J injury but even though hypoxaemia was not present 2,3-diphosphoglycerate values and P50 increased, compared with the control animals. The fall of plasma lipid concentrations reported probably had to be seen as a sympathomimetic effect of the minor (1.0 J) trauma. Of special significance was the increased activity of malate dehydrogenase and aldolase, found only in the blood of severely traumatized animals, as this could serve as an early diagnostic aid for evaluating head injuries.
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PMID:Biochemical and biophysical changes in guinea pigs after acute head injury. 0 Jul 49

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.
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PMID: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. 0 21

Beta adrenergic receptor antagonists (beta blockers) differ greatly in their cardioselectivity and intrinsic sympathomimetic activity, and these differences may have important therapeutic consequences. We have therefore studied the effect on blood pressure, heart rate and plasma renin activity of the beta blocking drug oxprenolol (Trasicor) which has considerable intrinsic sympathomimetic activity, both alone and in combination with the benzothiadiazine cyclopenthiazide. Eleven patients with mild to moderate benign essential hypertension were randomly allocated to one of two treatment groups. Oxprenolol was given as the first drug to Group 1, and cyclopenthiazide as the first drug to Group 2. The patients were assessed before the start of treatment, after 2 to 3 weeks of treatment with one drug and after a further 2 to 3 weeks of treatment with both drugs. Heart rate, blood pressure and plasma renin activity were measured with the patients recumbent and after a standardized tilt to 85 degrees to provide a reflection of day to day cardiovascular stress. Oxprenolol reduced arterial blood pressure without inducing significant bradycardia. The addition of cyclopenthiazide had little further effect. Oxprenolol alone suppressed plasma renin activity both at rest and during tilt and also abolished the increase in plasma renin activity after administration of cyclopenthiazide. The combination of (1) moderate reduction of blood pressure. (2) inhibition of the otherwise inevitable increase in plasma renin activity with the use of a diuretic drug, and (3) only moderate inhibition of overall sympathetic activity indicates that it is possible to achieve physiologic balance with the appropriate beta blocking drug.
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PMID:Beta adrenergic blockade and diuretic therapy in benign essential hypertension: A dynamic assessment. 0 63

Pretreatment with reserpine (0.3 or 3 mg/kg, 24 hours before the experiment) reduced the norepinephrine (NE) levels in the medial muscle of the cat nictitating membrane to approximately 2% of the control values. Under these experimental conditions, the responses to postganglionic nerve stimulation were not abolished, reaching up to 50% of the maximum development of tension to exogenous sympathomimetic amines both in vivo and in vitro. In contrast to the responses to nerve stimulation obtained in normal nictitating membranes, the residual responses to nerve stimulation obtained after pretreatment with reserpine were not blocked by phentolamine (3.1 and 31 muM) or by 0.29 muM phenoxybenzamine. The effectiveness of phentolamine and phenoxybenzamine in blocking responses to exogenous NE was the same when the normal nictitating membrane was compared to the smooth muscle obtained from cats pretreated with reserpine. The residual responses to nerve stimulation were reduced when the calcium concentration in the medium was decreased to 0.65 mM. These residual responses were abolished in the presence of tetrodotoxin. Scopolamine, 0.078 muM, did not reduce the residual responses to nerve stimulation while it antagonized the responses to exogenous acetylcholine, indicating that a cholinergic mechanism is not involved in this phenomenon. Adenosine triphosphate (ATP) and adenosine diphosphosphate (ADP) behaved as agonists on the smooth muscle of the normal and of the reserpine-pretreated nictitating membrane and the responses to ATP were not blocked by phentolamine. It is concluded that the residual responses to nerve stimulation obtained after pretreatment with reserpine could be due to the release of a transmitter different from NE. The possibility that ATP or ADP might be involved in these residual responses to nerve stimulation is discussed.
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PMID:Possible involvement of a transmitter different from norepinephrine in the residual responses to nerve stimulation of the cat nictitating membrane after pretreatment with reserpine. 0 7

The peripheral actions of beta-adrenoreceptor antagonists on adrenergic transmitter mechanisms have been reviewed. In addition to receptor blockade, beta-adrenoreceptor antagonists may in high concentrations inhibit neuronal uptake of noradrenaline; inhibit monoamine oxidase; inhibit the uptake of noradrenaline into transmitter storage vesicles and inhibit the extraneuronal uptake of noradrenaline. High concentrations of beta-adrenoreceptor antagonists (threshold about 30 muM) also release noradrenaline from intraneuronal stores; however, their intrinsic sympathomimetic activity is generally attributed to their partial agonist property. Beta-adrenoreceptor antagonists possess adrenergic neurone blocking activity and quinidine-like or local anaesthetic activity. The existance of a positive feedback mechanism involving prejunctional beta-adrenoreceptors is discussed. It is suggested that bradycardia produced by beta-adrenoreceptor antagonists is due to blockade of the action of circulating catecholamines or of transmitter noradrenaline at cardiac extrajunctional beta-adrenoreceptor sites.
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PMID:Effects of beta-adrenoreceptor blocking drugs on adrenergic transmission. 0 46

At the Dunedin Hypertension Clinic beta-blockers are the drugs of choice for most hypertensive patients, usually in combination with diuretics (especially in older subjects) and often with other drugs in the more severe cases. All beta-blockers have an antihypertensive effect, regardless of other characteristics (e.g. cardio-selectivity, instrinsic sympathomimetic effect, or membrane activity). d-Propranolol has no significant effect on blood pressure. Beta-blockers do not prevent stress-induced (mental arithmetic) rises in blood pressure in hypertensive subjects through the level of blood pressure reached during stress tends to be lower because the base line is lower. Twice-daily dosage of beta-blockers is usually satisfactory.
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PMID:Experience with beta-adrenoreceptor blockers in hypertension. 0 49

Lung function can be reduced not only by a non-selective beta-blocker but also by a selective beta1-receptor blocker. If both types of drug are without intrinsic sympathomimetic activity, the effect of the non-selective drug is more pronounced than that of a beta1-receptor selective drug under basal conditions. The effect of a beta2-receptor stimulating drug on the bronchi is inhibited by a non-selective drug, but much less by a selective beta1-receptor blocker. A selective beta1-receptor blocker can be used in asthmatics when it is combined with optimal anti-asthmatic therapy, while a non-selective drug is contra-indicated in patients with broncho-obstructive diseases. It is necessary to induce bronchodilatation (e.g. with a beta2-stimulator) in order to test whether or not a beta-blocker can be used in broncho-obstructive disease.
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PMID:Use of beta-adrenoreceptor blockers in combination with beta-stimulators in patients with obstructive lung disease. 0 50

Tha alpha-sympathomimetic agonists, clonidine, naphazoline, methoxamine, oxymetazoline and phenylephrine were used to further characterize the alpha-adrenoceptors mediating the positive inotropic effect in the isolated papillary muscle of the rabbit heart. The maximal inotropic effects of these amines were compared with the effect of isoprenaline and it was examined whether or not these amines compete for alpha-adrenoceptors. On the papillary muscle stimulated at 0.5 Hz, phenylephrine showed a high affinity (pD2 value=6.13) and produced the most pronounced intrinsic activity of the alpha-sympathomimetic amines. Therefore, the intrinsic activity of phenylephrine, in the presence of prindolol (3 X 10(-8) M), was used for comparison with those of the other alpha-agonists. Clonidine caused a positive inotropic effect: the intrinsic activity amounted to 0.32 of that of phenylephrine; the affinity was the highest among the amines tested (pD2 value=6.46); its effect was inhibited by 10(-6) M phentolamine. The affinity and the intrinsic activity of naphazoline were slightly lower than those of clonidine. Methoxamine showed a relatively high intrinsic activity (0.56) but the lowest affinity (4.68). Oxymetazoline did not cause any positive inotropic effect. Clonidine, naphazoline and oxymetazoline antagonized the positive inotropic effect of phenylephrine, mediated via the alpha-adrenocaptors in the presence of 3 X 10(-8) M prindolol, in a competitive manner. This observation suggests that these alpha-sympathomimetic amines compete with phenylephrine for the same receptor site. Thus the present results provide additional evidence for alpha-adrenoceptors mediating the positive inotropic actions of sympathomimetic amines in the rabbit papillary muscle.
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PMID:alpha-Adrenoceptors in the ventricular myocardium: clonidine, naphazoline and methoxamine as partial alpha-agonists exerting a competitive dualism in action to phenylephrine. 0 87

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.
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PMID:alpha-Adrenoceptors mediating positive inotropic effects on the ventricular myocardium: some aspects of structure-activity relationship of sympathomimetic amines. 0 94

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.
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PMID:[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)]. 0 63


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