Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The electrophysiological and mechanical effects of sotalol, a beta-adrenergic blocker with Class III antiarrhythmic properties, were compared with those of atenolol in rabbit right ventricular papillary muscles studied in vitro using intracellular microelectrodes. Sotalol produced a dose-dependent increase in action potential duration and effective refractory period without any effect on parameters of rapid inward current. Atenolol had no Class I or Class III effect. The actions of equipotent beta-blocking concentrations of sotalol (10(-4) mol X litre-1) and of atenolol (10(-5) mol X litre-1) in elevated extracellular potassium concentrations of 8 and 12 mmol X litre-1 were investigated. There were reductions in membrane potential, action potential amplitude and upstroke velocity in elevated potassium which were not influenced by sotalol and atenolol, apart from a small additional depression of action potential amplitude and membrane potential in 12 mmol X litre-1 potassium. Hyperkalaemia caused shortening in action potential duration but lengthening in effective refractory period (post-repolarisation refractoriness). The increase in effective refractory period over control produced by sotalol in normal potassium was preserved in elevated potassium. This effect was attributable to lengthening of action potential duration rather than alteration in the duration of post-repolarisation refractoriness. The Class III effects of sotalol are preserved even in partially depolarised fibres where rapid inward current is depressed.
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PMID:Effects of elevated extracellular potassium concentrations on the class III antiarrhythmic action of sotalol. 397 67

Episodes of depression and acute psychosis in two patients receiving propranolol hydrochloride are described, and the literature on propranolol-induced depression and psychosis is reviewed. A 42-year-old woman developed severe depression, marked apathy, social withdrawal, and anorexia after taking propranolol hydrochloride (80 mg/day) for three months to control her hypertension. Five days after the dose was reduced to 40 mg/day, there was a major improvement in her depressive symptoms, with a complete resolution in eight days. Upon rechallenge with 80 mg/day of propranolol, she again experienced depressive symptoms. Atenolol 50 mg/day was substituted for the propranolol therapy, and she exhibited a complete remission of her depression. The second patient was a 63-year-old man who had been taking propranolol hydrochloride 160 mg/day for three months without incident. Because of an increased frequency of anginal attacks, the dosage was increased to 240 mg/day. Within two days, he demonstrated such agitation, excitement, and combativeness that he had to be controlled with a 25-mg dose of methotrimeprazine. When the propranolol dose was reduced to 160 mg/day, his psychotic symptoms rapidly cleared. However, when the dose was subsequently increased to 200 mg/day, he again showed increased agitation. After substituting atenolol 100 mg/day for propranolol, the patient's mental status returned to normal. Both of these patients experienced symptoms that were temporarily associated with propranolol. Both patients were subsequently controlled without symptoms with atenolol therapy. Propranolol is a highly lipophilic beta blocker that achieves high concentrations in the brain. When continued beta-blocking therapy is necessary or beta blockade is indicated, a weakly lipophilic agent such as atenolol is indicated.
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PMID:Propranolol-induced depression and psychosis. 398 22

The aim of antiarrhythmic drug therapy is to terminate or suppress specific arrhythmias and improve cardiovascular function. Short-term studies of the new Class I drugs encainide, mexilitine, and tocainide have demonstrated only minor falls in cardiac index with modest rises in mean aortic pressure. In contrast, disopyramide has been shown to depress myocardial function in both animals and patient studies. Heart failure may be precipitated by therapy with disopyramide and electromechanical dissociation has been reported. Class II agents with beta-adrenergic blocking actions all produce a degree of myocardial depression. Atenolol resembles propranolol in patients with coronary artery disease in its hemodyanmic effects, whereas acebutolol is less of a depressant, resembling practolol. The Class III agent amiodarone has only a mild depressant effect associated with a reduction in afterload and an increase in coronary blood flow. The Class IV agent verapamil, which is a calcium channel blocker, has potent myocardial depressant actions and causes peripheral vasodilatation. Hypotension, heart failure, and shock have been precipitated particularly in patients receiving beta-blocking drugs concurrently. While all the new antiarrhythmic drugs currently studied will cause some degree of hemodyanmic depression in an appropriately high concentration, present investigations suggest that particular caution needs to be taken when disopyramide, aprindine, atenolol, and verampamil are administered either acutely by the intravenous route or chronically by the oral route.
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PMID:Hemodynamic effects of newer antiarrhythmic drugs. 677 96

Thirty patients with stable angina have been undergone a multistage treadmill test, after a single oral dose of 100 mg of Atenolol, a beta 1 . selective blocking agent, in comparison to a previous test carried out after an identical looking placebo tablet. After placebo all the patients showed ischemic ST segment response (ST depression greater than 1 mm), 25 of them interrupting the test because of anginal pain (20 patients), or of ST depression greater than 3 mm (3 patients), or of ventricular ectopics (one patient), or of fatigue (one patient). After Atenolol 10 patients completed the planned test, 7 of them without ischemic changes of ST. 27 patients (90%) showed increased working capacity with significant reduction of heart-rate (FC), systolic blood pressure (PAS) and their product and of ST depression, either before and during and at the end of exercise. The recovery time of ischemic ECG change has been significantly reduced. The observed increased working capacity is attributed to the reduced myocardial O2 consumption expressed from the reduction of the product FC x PAS. Nevertheless at the end of exercise test after beta-blocking drug this product didn't reach the threshold value at which the test was interrupted in the first test after placebo. The authors discuss the possible cause of this effect of beta-blocking drugs, which could be attributed to a reduction of coronary blood flow and/or to an increased myocardial tension because of increased end diastolic ventricular volume. However the Authors outline that the per cent increases of FC, PAS, and FC x PAS have not been reduced by the Atenolol, unlike their absolute values, at the threshold of angina: the ischemic reveals itself at same levels of per cent increase of the factors of O2 myocardial consumption, the later reaching of threshold values depending on the lower starting values. The advantages of Atenolol as regards the other beta-blocking drugs (better acceptability, stability and duration of action) are outlined too.
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PMID:[Evaluation by exercise test of effects of a single oral dose of atenolol in patients with stable angina (author's transl)]. 704 18

Atenolol has been studied prospectively in the management of ten patients with essential hypertension during pregnancy. Median supine BP fell significantly from 156/98 mmHg before treatment to 128/82 mmHg at term. Atenolol did not suppress cardiotocographic signs of foetal distress. Although there was one intrauterine death, the remaining nine babies had a median Apgar score at birth of 9 and a median weight which was 82% of the gestational mean. There were no cases of neonatal bradycardia or respiratory depression and the only case of hypoglycaemia was in a dysmature baby. These findings justify a formal study of beta-adrenoceptor blocker therapy in hypertensive diseases of pregnancy.
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PMID:Atenolol in the treatment of essential hypertension during pregnancy. 710 79

1 The pharmacological properties of atenolol suggest its possible usefulness in pregnancy-induced hypertension. The pharmacokinetics of atenolol in the pregnant woman, concentrations in cord blood, and its effects on maternal blood pressure and the foetus, are evaluated. 2 We studied 13 pregnant women with hypertension, most of them uncontrolled on methyldopa. Whole blood concentrations and urinary excretion of the drug were measured over 24 h following a 100 mg dose. Effects on maternal blood pressure, pulse rate and foetal heart rate and cardiotocograph were compared for the 4 days before treatment and the first 4 days of treatment. The birth weights and Apgar scores of the babies were recorded. 2 The pharmacokinetics of atenolol (plasma half-life of about 8 h) in pregnant women do not differ from the findings in the non-pregnant. The levels of atenolol in the cord blood were confirmed as approximately equal to those in the maternal blood. 4 In the ten women in whom blood pressure was assessed a small significant fall in blood pressure was observed. 5 A 5% mean fall in foetal heart rate resulted but in one case was a rate below 120 beats/min recorded. There was no evidence of depression of the stress response of the foetal heart. Apgar scores 5 min post partum were satisfactory. 6 Atenolol appears to be safe for use in hypertensive pregnancies. Its effectiveness as an antihypertensive agent in pregnancy requires further controlled evaluation.
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PMID:Atenolol in the treatment of pregnancy-induced hypertension. 733 38

The gastrointestinal therapeutic system formulation of nifedipine enables a once-daily dosing resulting in predictable, relatively constant plasma concentrations. To evaluate the efficacy and safety of this formulation and to compare this with the beta-blocker atenolol, we conducted a double-blind, randomised, multi-centre study in 129 male patients with documented exercise induced angina pectoris. After 4 weeks' treatment, nifedipine (60 mg), improved time to onset of 0.1 mV ST-segment depression from 536 s by 72 +/- 117s, time to onset of pain from 619 s by 56 +/- 120 s, and total exercise time from 685 s by 40 +/- 88 s. Atenolol 100 mg, had a comparable effect, time to onset of 0.1 mV ST-segment depression improved from 496 s by 53 +/- 129 s, time to onset of pain from 572 s by 57 +/- 118 s, and total exercise time from 653 s by 33 +/- 99 s. Between group analysis revealed no statistically significant differences for these exercise parameters. Atenolol, but not nifedipine, significantly reduced heart rate and systolic blood pressure at rest and during exercise (P < 0.001 between groups), indicating different modes of action of the drugs. With regard to safety, both drugs were generally well tolerated. There were significantly (P = 0.01) more vasodilation related side effects with nifedipine. These data demonstrate that gastrointestinal therapeutic system formulation of nifedipine and atenolol as once-daily monotherapy are equally effective and safe, but with different effects on exercise parameters.
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PMID:Nifedipine gastrointestinal therapeutic system versus atenolol in stable angina pectoris. The Netherlands Working Group on Cardiovascular Research (WCN). 901 66

To confirm the usefulness of head-up tilt test (HUT) in neurocardiogenic syncope (NCS) with complicating clinical features, retrospective analysis were done on 12 selected children. The age at onset was 12.7 +/- 1.9 (mean +/- SD) years. Associated clinical features were postoperative congenital heart disease (PO CHD) in 3, coexistent arrhythmia in 8 (persistent ventricular arrhythmia during exercise in 3, premature ventricular contractions in 2, ventricular couplets in 1, sinoatrial exit block in 1 and resting sinus bradycardia in 1) and ST segment depression during exercise in 1. Four of them had a history of exercise-related syncope. All 3 patients with PO CHD had arrhythmia (ventricular tachycardia in 1, sinus bradycardia in 1 and atrioventricular block in 1). HUT provoked NCS in 8 (2 during baseline tilt, 6 during isoproterenol infusion). In one each, ventricular tachycardia and loss of consciousness without hypotension and bradycardia were induced. Atenolol was tried in 5 with improvement of NCS in 4 and aggravation of dizziness in 1. During follow-up, 7 became asymptomatic (2 with atenolol) and 5 were stationary. In conclusion, HUT was valuable in diagnosing NCS even in children with complicating clinical features such as arrhythmias or PO CHD. HUT could be done as apart of initial diagnostic tests if the past history suggests NCS, regardless of associated clinical features. In some cases, the unexpected results of the test turned out useful in managing children with syncope or dizziness.
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PMID:Head-up tilt test in complicated neurocardiogenic syncope in children. 914 59

This double-blind, randomised multicentre study compares nifedipine gastrointestinal therapeutic system (GITS) with atenolol in 129 male patients, with exercise-induced angina pectoris. At 4 weeks, there was no significant difference between nifedipine GITS 60 mg o.d. and atenolol 100 mg o.d., in respect of improved time to onset of 0.1 mV ST-segment depression, time to onset of pain, and total exercise time. Atenolol, but not nifedipine, significantly reduced heart rate and systolic blood pressure at rest and during exercise. There were significantly more vasodilator-related side effects with nifedipine. Nifedipine GITS and atenolol as once-daily monotherapy are equally effective and safe, but have different effects on exercise parameters.
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PMID:Monotherapy with nifedipine GITS compared with atenolol in stable angina pectoris. The Working Group on Cardiovascular Research (WCN). 951 1

Forty outpatients suffering from angina pectoris due to coronary artery disease and concomitant reversible. chronic obstructive bronchitis were treated with the beta1-selective beta-blockers atenolol (50 mg) and bisoprolol (5 mg) for 6 months in each case, following a randomized, double-blind crossover study design. Lung function tests were carried out by means of whole-body plethysmography before and then several times during treatment. 2 to 4 h after drug intake (once daily in the morning). The main target variables for the factorial analysis of variance for comparison of the two beta-blockers were the airway resistance (AWR), the forced expiratory volume in the first second (FEV1), and the peak expiratory flow rate (PEFR). Bicycle ergometry was performed before and after therapy in order to check the cardiovascular effects of the two beta-blockers. The patients were questioned as to their angina pectoris and bronchitis symptoms at the monthly check-ups. There was no difference between the two beta-blockers (p > 0.05), both causing a slight increase in AWR, which increased with therapy duration, and a small but significant decrease in FEV1 and PEFR (p < 0.01). The bronchitis symptoms were not affected; however, seasonal influences were detected. Atenolol and bisoprolol had comparably pronounced effects on the cardiovascular parameters during ergometry (blood pressure, heart rate, W x min product, and ST-segment depression) and the frequency of angina pectoris attacks. Even beta1-selective beta-blockers may cause an impairment of lung function in patients with chronic obstructive bronchitis. This may be due to the presence of beta1-adrenoceptors in the bronchial tissue. Fifty milligrams of atenolol and 5 mg of bisoprolol once per day are effective in the treatment of angina pectoris.
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PMID:Long-term treatment of angina pectoris with bisoprolol or atenolol in patients with chronic obstructive bronchitis: a randomized, double-blind crossover study. 1152 35


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