Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three beta-adrenoceptor mediated effects were measured in vitro on tissues from guinea-pig: (a) relaxation of the trachea (mainly beta 2), (b) increase in the force of contraction of the papillary muscle (beta 1), and (c) depression of the subtetanic contractions of the soleus muscle (beta 2). The relaxant effect of ephedrine on the trachea was weak but was resistant to reserpine pretreatment. There was no appreciable agonistic effect of ephedrine on the soleus muscle. Ephedrine per se had a marked positive inotropic effect on the papillary muscle with a pD2 of about 6.0. This effect disappeared completely after pretreatment with reserpine. Ephedrine inhibited the response to isoprenaline. The apparent pA2 was about 4.8 in all tissues studied.
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PMID:The interaction of ephedrine with beta-adrenoceptors in tracheal, cardiac and skeletal muscles. 300 91

The hemopoietic effects of glucan, a beta 1,3 polyglycan biological response modifier, were assayed in normal and irradiated mice. In normal mice, glucan administration increased the content of bone marrow and splenic transplantable pluripotent hemopoietic stem cells (CFU-s), committed granulocyte-macrophage progenitor cells (GM-CFC), and pure macrophage progenitor cells (M-CFC). In mice partially hemopoietic depleted by exposure to 6.5 Gy of 60Co irradiation glucan increased the number of endogenous pluripotent hemopoietic stem cells (E-CFU). The most pronounced effects were observed when glucan was administered 1 day before irradiation. In addition, the administration of glucan 1 day before lethal (9.0 Gy) irradiation-enhanced survival. The enhanced survival in glucan-treated mice in part appeared to be mediated by an enhanced resistance to the surgence of enteric opportunistic pathogens that occurs following radiation-induced hemopoietic and immune depression.
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PMID:Glucan-induced hemopoietic and immune stimulation: therapeutic effects in sublethally and lethally irradiated mice. 371 78

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 +/- 8.4 to 178.5 +/- 11.3 mmHg (P less than 0.01) and left ventricle end-diastolic pressure from 3.5 +/- 0.7 to 8.9 +/- 1.0 mmHg (P less than 0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 +/- 1.9 to 4.80 +/- 1.2 ms/mmHg (P less than 0.01) for the pulse interval relationship and from -2.51 +/- 0.53 to -1.14 +/- 0.32 beats . min-1 . mmHg-1 (P less than 0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. beta 1-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs. 372 8

Recent evidence has linked alpha-receptor and beta-receptor activations with ventricular arrhythmia genesis. In order to assess the relative contribution of specific adrenoceptors (alpha 1, alpha 2, beta 1) on ventricular arrhythmogenic activity during xylazine (1.1 mg X kg-1 X hr-1)-halothane (1.35%) anesthesia, the arrhythmogenic dose of epinephrine (ADE) was repeatedly determined before and after prazosin (alpha 1 antagonist; 0.1 mg X kg-1), metoprolol (beta 1 antagonist; 0.5 mg X kg-1), and yohimbine (alpha 2 antagonist; 0.125 mg X kg-1) administration in 6 dogs. The ADE was expressed as infusion rate and total dose. The ADE was defined as the dose which produced 4 or more intermittent premature ventricular contractions within 15 s during a 3-minute infusion period or within 1 minute from end of infusion. Control ADE was 2.69 +/- 0.372 (micrograms X kg-1 X min-1) and 4.17 +/- 0.544 (micrograms X kg X -1) for infusion rate and total dose, respectively. The ADE significantly increased after prazosin (P less than 0.005), metoprolol (P less than 0.005), and yohimbine (P less than 0.05) administration. The ADE values increased to 5.42 +/- 1.22 (rate) and 8.10 +/- 1.95 (dose) after alpha 2 blockade, but were significantly less than the alpha 1 and beta 1 blockade ADE values. In conclusion, although both alpha- and beta-adrenoceptor blockade depressed ventricular arrhythmia genesis in xylazine-halothane-anesthetized dogs, alpha 2 blockade, which was achieved with the recommended dose of yohimbine for reversal of anesthetic-induced CNS depression, was not as protective as alpha 1 (prazosin) or beta 1 (metoprolol) blockade.
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PMID:Alterations in the arrhythmogenic dose of epinephrine after adrenergic receptor blockade with prazosin, metoprolol, or yohimbine in halothane-xylazine-anesthetized dogs. 394 87

Left ventricular function was studied in 15 patients both before and after intravenous administration of Practolol (an agent blocking selectively the heart beta-adrenergic receptors (beta 1)), while the heart rate was constant by right atrial pacing. The negative inotropic effect linked to the negative chronotropic effect of the beta-adrenergic blockage, represented approximately one quarter of the overall depression of the contractility. Right atrial pacing determined a decrease of the left ventricular end-diastolic pressure and an increase of the pacing rate by 20% above the spontaneous heart rate, after administration of 30 mg of Practolol, brought the contractility back to its control level.
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PMID:[Effects of selective beta adrenergic block on myocardial contractility. Relative role of negative inotropic and chronotropic effects]. 421 30

Alpha 1, alpha 2, beta 1 and beta 2 adrenergic receptors were measured in the pre-frontal cortex of parkinsonian patients post-mortem. The number of beta 2 receptors was the same in control and parkinsonian subjects. alpha 1 and beta 1 receptors increased in number, particularly in demented parkinsonian patients, while alpha 2 receptors decreased. The affinity constants were unchanged. The modifications seem to be related to lesion of the noradrenergic pathway from the locus coeruleus to the cortex. The relationship between this lesion and the symptoms of dementia and depression in parkinsonian patients is discussed.
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PMID:Adrenergic receptors in Parkinson's disease. 609 67

beta-Adrenoceptor-blocking agents constitute a heterogeneous group of compounds. Membrane- stabilizing (quinidine-like) effects can be demonstrated pharmacologically with most compounds, but only at relatively high concentrations. There is no evidence to suggest that this property is of clinical relevance. Some compounds have a certain selectivity for receptors of the beta 1-type, whereas others possess beta-adrenoceptor stimulant activity (partial agonism). The clinical importance of these latter properties remains controversial. The selectivity for beta 1-adrenoceptors, which can be demonstrated pharmacologically for atenolol, metoprolol, and practolol, appears quite broad. Nevertheless a clear advantage over nonselective compounds with respect to their effects on lung function and vascular resistance in patients has not been established. There are two possible explanations. The first is that the doses used therapeutically may lie outside the selective range; the second is that most tissues appear to possess and mixed population of beta 1- and beta 2-adrenoceptors. According to our present understanding, even absolute specificity for a given subtype cannot provide organ or tissue specificity. Partial agonists provide a constant stimulation of beta-adrenoceptors while at the same time preventing access of catecholamines to the receptor they occupy. With some compounds (e.g., pindolol), stimulant activity may be sufficient to counterbalance the myocardial depression normally resulting from blockade of basal sympathetic tone. Heart rate and cardiac output are thus maintained within normal limits and compensatory increases in vasomotor tone (seen with antagonists lacking intrinsic activity) do not occur. Pindolol has been shown to dilate blood vessels at very low doses and to produce significant relaxation of isolated tracheal smooth muscle at concentrations within the range of therapeutic plasma levels found in humans. These effects may underly the relatively low incidence of bronchopulmonary and vascular side effects reported for this compound.
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PMID:Beta-adrenoceptor-blocking agents: are pharmacologic differences relevant? 612 93

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.
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PMID:Beta-adrenoceptor blockade and atrio-ventricular conduction in dogs. Role of intrinsic sympathomimetic activity. 612 66

Intravenous beta-blocking drugs are being increasingly used in early myocardial infarction but little is known of the comparative haemodynamic effects of drugs with different ancillary pharmacological properties. In patients with stable coronary heart disease all intravenous beta-blocking drugs reduce left ventricular pumping function in a dose-response fashion. The reduction in cardiac mechanical activity is directly related to the dose and inversely related to the degree of intrinsic sympathomimetic activity possessed by each drug; it is independent of the property of 'cardioselectivity'. The lesser depression of left ventricular pumping performance after beta-blocking drugs with intrinsic sympathomimetic activity is probably due to two primary pharmacodynamic effects: a) increased myocardial contractile activity due to stimulation of post-synaptic beta 1- and presynaptic beta 2-adrenoceptors in the sinus node and ventricular myocardium; b) reduction in left ventricular afterload consequent upon the fall in systemic vascular resistance resulting from stimulation of vasodilator beta 2-adrenoceptors in peripheral resistance vessels. A similar but less marked haemodynamic separation of beta-blocking drugs with and without intrinsic sympathomimetic activity is observed in patients with acute myocardial infarction. The quantitative difference in the haemodynamic effects of intravenous beta-blocking drugs in angina pectoris compared to their effects in acute myocardial infarction is probably due to the higher level of sympathetic stimulation and sensitivity to beta-blockade in the latter. It has yet to be shown by formal clinical trial that the haemodynamic advantages attributable to the possession of intrinsic sympathomimetic activity by a beta-blocking drug are translated into clinical benefit.
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PMID:Haemodynamic effects of intravenous beta-blocking drugs in coronary heart disease. 613 65

L-3,4-(3-3,4-Dimethoxyphene-ethylamino-2-hydroxypropoxy)-phenyl-++ +crotonic acid nitrile X HCl (Hoe 224) has beta 1-blocking action. In the isolated left atrium of the guinea pig, the ED50 necessary to counteract the positive inotropic action of 2 ng/ml isoprenaline (isoproterenol) was determined as 10.3 ng/ml in comparison to the ED50 of propranolol 2.7 ng/ml. On the isolated right atrium of the same animal, the ED50 for inhibition of increased heart rate brought about by 2 ng/ml isoprenaline was 29.5 ng/ml in comparison to the ED50 of propranolol 13.5 ng/ml. On the isolated tracheal chain of the guinea pig 40 micrograms Hoe 224/ml also inhibited relaxation induced by 50 ng isoprenaline/ml only by 31%. The ED50 for propranolol in this experiment was 1.2 ng/ml. Therefore, Hoe 224 is a very specific beta 1-blocker. In the dog anaesthetized with pentobarbital the ED50 of Hoe 224 for depression of dp/dt increase by 0.1 mg isoprenaline/kg i.v. was determined as 85 micrograms/kg i.v. Under the same conditions, the ED50 for propranolol was 10 micrograms/kg i.v., for atenolol 17 micrograms/kg i.v., for practolol 56 micrograms/kg i.v. In the conscious dog, 1.6 mg Hoe 224/kg orally depressed the increase of dp/dt brought about by 0.1 microgram isoprenaline/kg i.v. by 50%. The beta 2-blocking effect of Hoe 224 intraarterially against vasodilating effect of 0.01 microgram isoprenaline/kg given intraarterially in the A. femoralis of anaesthetized dogs was very weak. 100 micrograms Hoe 224/kg reduced the effect of isoprenaline only by 23%, but 2 micrograms propranolol/kg intraarterially reduced this effect by 61%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:L-3,4-(3-3,4-dimethoxyphenethylamino-2-hydroxypropoxy)-phenyl- crotonic acid nitrile.HCl (Hoe 224), a beta-blocking agent with high beta 1-selectivity. 614 30


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