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At least 19 recordsLinked to original sources
PubMed1978

Comparison of atenolol with propranolol in the treatment of angina pectoris with special reference to once daily administration of atenolol.

Fourteen patients with angina pectoris completed a double blind trial of atenolol 25 mg, 50 mg, and 100 mg twice daily and propranolol 80 mg thrice daily. In comparison with placebo, all active treatments significantly reduced anginal attacks, consumption of glyceryl trinitrate, resting and exercise heart rate, resting and exercise systolic blood pressure, and significantly prolonged exercise time. There was no significant difference between the effects of propranolol and atenolol. Nine patients completed a further trial comparing atenolol given once or twice daily. Both regimens were effective and there was no significant difference between the reductions in anginal attacks, glyceryl trinitrate consumption, systolic blood pressure, or heart rate. Twenty-four-hour ambulatory electrocardiograms showed that atenolol consistently reduced heart rate throughout the 24-hour period whether given once or twice daily. Atenolol is a potent antianginal agent which, in most patients, is likely to be effective once daily.

Adult↗
PubMed1979

The effects of a beta 1-blocking agent, atenolol, on blood pressure, plasma renin activity and prostaglandin F2 alpha excretion in patients with essential hypertension.

The antihypertensive action of beta-blocking agents has been suggested to be associated with the decrease in plasma renin activity (PRA) and can be antagonized by indomethacin, a prostaglandin (PG) synthesis inhibitor. We studied the acute and long-term effects of a beta 1-blocking agent, atenolol (50 mg b.i.d.), on blood pressure (BP), PRA and urinary PGF2 alpha excretion in 12 male patients (40 years old) with essential hypertension. BP was measured by means of a brachial cuff. PRA and PGF2 alpha were estimated radioimmunologically. One day after the initiation of atenolol treatment, BP fell significantly, the supine values from 159/114 to 143/104 mmHg and the erect from 158/118 to 140/106 mmHg. In six weeks BP decreased further to 135/94 and 134/96 mmHg, respectively. After the cessation of atenolol for three weeks BP rose to the pre-atenolol level. When the dose was readjusted (25-150 mg daily for 26 weeks), diastolic BP remained at 100 mmHg or higher in only two patients. During the atenolol treatment PRA declined to one-third of the pre-atenolol level in one day and to one-half in six weeks. The urinary excretion of PGF2 alpha was not affected by atenolol. Our results suggest that 1) the antihypertensive action of atenolol and the reduction of PRA are substantial already in one day, and 2) the decrease in BP or PRA is not associated with PGF2 alpha production.

Adult↗
PubMed1978

Atenolol versus adrenaline eye drops and an evaluation of these two combined.

In a 1-day, 1-dose, double-masked, randomised trial, with each of 12 patients acting as his/her own control, atenolol drops 4% (a selective beta1-adrenergic blocker) produced a significantly greater fall in ocular tension measured by applanation than did adrenaline drops 1% (P is less than 0.01 Wilcoxon matched pairs signed ranks test). The mean differences, which favoured atenolol, between the falls in pressure produced by these 2 drugs at 1.5 hours, 3.5 hours, 5.5 hours, and 7 hours after instillation of the drops was 2.1, 4.6, 4.0, and 3.6 mmHg, respectively. Long-term studies would be required before any conclusion was justified about the relative merits of these 2 drugs in the treatment of glaucoma. There was no significant difference between the ocular hypotensive effects of atenolol-then-adrenaline and adrenaline-then-atenolol. It was disappointing that the expected adjuvant effect of atenolol's preceding adrenaline was not found-rather the reverse. Atenolol alone, however, was significantly better than atenolol-then-adrenaline (P is less than 0.02 Wilcoxon matched pairs signed ranks test), and there was also some indication that it was superior to adrenaline-then-atenolol. The response to adrenaline did not differ markedly from the response to the combination in either order.

Atenolol↗
PubMed1979

Atenolol and chlorthalidone on blood pressure, heart rate, and plasma renin activity in hypertension.

The antihypertensive effect of atenolol, with and without chlorthalidone, on hypertension was assessed in an outpatient as well as in an inpatient study. In the outpatient study atenolol alone induced decreases in systolic and diastolic BP amounting to 20 and 15 mm Hg. Maximal response of BP and HR developed within a week at the lowest dose used (100 mg twice daily). Combined atenolol-chlorthalidone treatment decreased lying and standing systolic BP by 7 and 14 mm Hg more than atenolol alone, but diastolic BP was decreased little more. In the inpatient study the addition of atenolol to chlorthalidone therapy in a dose of 100 mg twice daily resulted in a maximal decrease in BP within 3 days. At this dose PRA was lowered only slightly. Larger doses did not lead to any significant further decrease in BP, whereas PRA fell progressively. Our results indicate that, in contrast to nonselective blockade, specific beta-1-adrenoceptor blockade by atenolol is capable of inducing a distinct antihypertensive effect, unrelated to suppression of PRA. The decrease in PRA after larger doses of atenolol was not accompanied by a further decrease in BP. Because diuretic-induced renin release plays a role in the maintenance of the BP, our findings suggest that at higher dosages a hypertensive effect of the beta blocker compensated for the hypotensive effect of the decrease in PRA.

Adult↗
PubMed1979

Effects of atenolol and propranolol when added to long-term antihypertensive diuretic therapy.

The antihypertensive effects of atenolol and propranolol were compared in a double-blind crossover study of 19 patients with essential hypertension (World Health Organization, I and II) who were receiving long-term diuretic treatment (chlorthalidone, 50 mg daily) during the study. After a 3-wk placebo period, a beta-adrenergic antagonist was administered once daily (atenolol, 50 mg daily, or propranolol, 80 mg daily) for a week. If the MAP was more than 108 mm Hg at the end of the week, dosage of the beta-blocker was doubled the following week; when necessary, doubling was repeated to a maximum dose of 640 mg propranolol and 400 mg atenolol daily. Fifty milligrams atenolol had a greater effect than 80 mg propranolol and was as effective as 160 mg propranolol. The dose-response curve flattened off after 160 mg propranolol and 50 mg atenolol daily. The two highest doses of atenolol lowered MAP more than the highest doses of propranolo. Heart rate slowing was the same for both drugs and did not correlate with the fall in blood pressure. PRA was suppressed by all doses of propranolol, whereas atenolol suppressed PRA only at the 2 highest doses, (200 and 400 mg daily). With the lower propranolol doses, the percent MAP change correlated weakly with the percent PRA change (80 mg--r = 0.41, p less than 0.1; 160 mg--r = 0.64, p less than 0.05). Side effects were minimal, and were noted only with 640 mg propranolol; with this exception, the percentage of patients with no complaints rose when placebo was replaced by beta-blockers.

Administration, Oral↗
PubMed1978

Penetration of atenolol in the rabbit eye.

The ocular penetration of topically applied [14C]-atenolol in the rabbit was determined by means of liquid scintillation counting. Only one eye was treated, the fellow eye serving as a control. Blood plasma levels were measured as well. The absolute amount of atenolol which penetrated the eye was very low, but a relatively high concentration was achieved in the tissues of the nictitating membrane. We could only detect an increase in the amount of atenolol with time in the aqueous humor. In all other ocular tissues, including iris and ciliary body, the atenolol level remained constant with time. Hardly any atenolol could be detected in the untreated eye and none in the blood plasma. These findings suggest that the ocular penetration of atenolol administered as an eye drop is very poor. Ocular penetration, therefore, hardly seems to play a part in the antiglaucomatous effect of atenolol.

Animals↗
PubMed2026

Effect of atenolol versus ivabradine on heart rate variability in patients of schizophrenia with clozapine-induced tachycardia: a randomized controlled trial.

BACKGROUND: A third of schizophrenia cases are resistant to antipsychotics, where clozapine is the only FDA-approved medication. Clozapine use is often limited by intolerable adverse effects. Persistent tachycardia occurs in approximately 25-54% patients receiving clozapine. Heart rate variability (HRV) is a non-invasive, clinically relevant marker of autonomic nervous system functioning. Atenolol and Ivabradine are usually prescribed for clozapine-induced tachycardia (CIT), although evidence guiding their optimal use remains limited. AIM: This study aimed to compare the effects of atenolol versus ivabradine on HRV in patients with treatment-resistant schizophrenia (TRS) receiving clozapine. METHODS: This open-label randomised clinical trial, conducted at a tertiary-care center over 20 months, involved TRS patients on clozapine for more than three months and having persistent tachycardia. Twenty patients received atenolol 25mg once-daily, while twenty received ivabradine 5mg twice-daily for two months. The primary outcome was the change in the frequency domain of HRV, while the secondary outcomes were time-domains, central and peripheral blood pressure, pulse rate and treatment-emergent adverse events (TEAE). RESULTS: While both drugs significantly reduced pulse-rates (atenolol: -20.56&#xb1;13.00, p<0.001; ivabradine: -21.855&#xb1;12.873, p<0.001). Within-group analysis showed that, the atenolol group had significant improvements in high-frequency [HF] power (p=0.048) and LF/HF ratio (p=0.044), along with a non-significant trend towards increased total power (p=0.053); no significant within-group changes were observed in the ivabradine group. CONCLUSION: No significant between-group differences in HRV parameters were established between atenolol and ivabradine. Ivabradine could be a viable option in patients where atenolol is either contraindicated or not tolerated. Future larger multicentric studies are needed for greater generalisability. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT06505668.

Humans↗
PubMed1977

Atenolol in the treatment of angina pectoris.

Nineteen men, aged 41-64 years, with stable angina pectoris have completed a random double-blind study of atenolol, 50 mg b.i.d., atenolol, 100 mg b.i.d., and placebo. Fifteen patients had subjective improvement on atenolol, two were unchanged and two felt worse (because of asthenia/leg fatigue). No significant placebo effect was found. On both atenolol dosages there were highly significant reductions in heart rate at rest and during exercise and in BP. Only the maximal heart rate decreased significantly more on 100 mg atenolol than on 50 mg (p less than 0.01). Fourteen patients had the same or a better physical performance on the 50 mg b.i.d. regimen than on the 100 mg b.i.d. regimen, although this difference was not significant. Sixteen patients had higher bicycle exercise performance on atenolol than on placebo. Disregarding the three non-responders, a mean increase of 44% in bicycle performance was found. No serious side-effects were seen. Most individuals reported an increased feeling of well-being on atenolol.

Adrenergic beta-Antagonists↗
PubMed1979

Home blood pressure monitoring and changes in plasma catecholamines during once or twice daily treatment with atenolol in patients with mild hypertension.

1. The effects of atenolol on diurnal blood pressure control, heart rate and plasma catecholamines were studied in nine hypertensives, six of whom also received diuretics. The patients completed a double-blind trial in which the effects of once and twice daily administration of atenolol were compared with placebo. 2. Atenolol (100 mg) given once a day produced significant reduction in diurnal blood pressures recorded at home but the effect was slightly less than either 50 mg given twice a day or 200 mg once a day. 3. Effects on heart rate and blood pressure were seen within 36 hours of the first dose, and were near maximal at 72 hours. After cessation of the drug, mean resting heart rate increased gradually and reached pre-treatment levels five days later, suggesting strong tissue binding of atenolol. Blood pressure increased more slowly over 8--10 days. 4. Plasma noradrenaline levels were increased at rest with atenolol. This argues strongly against the antihypertensive effect of atenolol being due to a reduction of sympathetic nerve activity. 5. Once daily administration of atenolol in this group of patients with mild hypertension produced satisfactory diurnal blood pressure control and beta blockade without "rebound" hypertension on cessation of therapy.

Adult↗
PubMed1979

Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension.

Atenolol is a beta-selective (cardioselective) adrenoceptor blocking drug without partial agonist or membrane stabilising activity. Its profile of action most closely resembles that of metoprolol which differs only in that it has some membrane stabilising activity. Atenolol has been well studied and is effective in the treatment of hypertension and in the prophylactic management of angina. Its narrow dose response range obviates the need for highly individualised dose titration. In patients with angina its long duration of beta-blocking activity allows once daily dosage, whereas other beta-blockers, unless in sustained release dosage forms, need to be given in divided doses. Other beta-blockers can be given once daily in hypertension, but at presnt the evidence for effective control with a once daily regimen is more convincing with atenolol. Further studies are need to clarify any important differences in blood pressure control between the various beta-blocking drugs, both in conventional or sustained release dosage forms. As with metoprolol, atenolol is preferable to non-selective beta-blockers in patients with asthma or diabetes mellitus. Atenolol has been well tolerated in most patients, its profile of adverse reactions generally resembling that of other beta-blocking drugs, although its low lipid solubility and limited penetration into the brain results in a lower incidence of central nervous system effects than seen with propranolol. Atenolol is eliminated virtually entirely as unchanged drug in the urine and dosage needs to be reduced in patients with moderate to severely impaired renal function (glomerular filtration rate less than 30 ml/min). There is no need for modification of dosage of atenolol in liver disease.

Adrenergic beta-Antagonists↗
PubMed1978

Metabolism of atenolol in man.

1. The disposition and metabolism of 1-(4-carbamoyl[14C]methylphenoxy)-3-isopropylaminopan-2-ol (atenolol, Tenormin) has been studied in man following oral and intravenous doses. 2. Approx. 50% of an oral dose was eliminated in urine; the major radiolabelled component was atenolol (approx. 90%). Faecal extracts also contained largely unchanged atenolol, with small amounts of more polar metabolites. Biliary excretion of atenolol and its metabolites is not a major route of elimination in man. Metabolism of the compound is not extensive and route-dependent modes of metabolism do not appear to complicate the position. 3. Atenolol appeared to be the only major radiolabelled component in blood. 4. Oral doses of atenolol are incompletely absorbed (range 46-62%), even when formulated as a solution. 5. 1-[4-(C-Carbamoylhydroxymethyl)phenoxy]-3-isopropylaminopropan-2-ol was a minor urinary metabolite, which has only one tenth the activity of the parent compound as a beta-adrenergic blocking agent in the rat. 6. Pharmacological activity in man appears to be due to atenolol alone.

Administration, Oral↗
PubMed1979

[Atenolol in the treatment of angina pectoris].

18 patients with angina pectoris participated in a double blind trial with atenolol (100 mg and 200 mg once daily, or 100 mg twice daily) and propranolol (80 mg twice daily). The number of anginal attacks (NAP), the number of days free of pain (NAFT), consumption of sublingual nitroglycerin (NNT) and bicycle ergometry data (EFE) were recorded. Atenolol given in a dose of 100 g twice daily significantly reduced NAP and NNT as compared with the other dose schedules for atenolol and propranolol. There was, however, no difference between NAFT and EFE under any of the treatment schedules mentioned above. Only with 100 mg atenolol twice daily was it possible to reduce heart rate at rest and immediately after exercise testing, and also diastolic blood pressure (at rest, upright and after stress testing). In spite of the long plasma T 1/2 (= 24 hours) reported by others, atenolol given twice daily seems to be the most effective schedule. It is concluded that atenolol (100 mg twice daily) has a more potent anti-anginal effect than propranolol (80 mg twice daily). In addition, atenolol has the advantage of being cardioselective.

Aged↗
PubMed1977

Contribution of atenolol, bendrofluazide, and hydrallazine to management of severe hypertension.

The efficacy of various combinations of atenolol, bendrofluazide, and hydraliazine given twice daily was assessed in a double-blind trial on 39 patients with moderate to severe essential hypertension. Concurrent treatment with all three drugs proved most effective and produced a mean reduction in blood pressure of 43/31 mm Hg. In the dosage used, hydrallazine affected only the diastolic blood pressure, and when added to either bendrofluazide or bendrofluazide plus atenolol it produced a further mean reduction in pressure of 6 mm Hg. Once-daily treatment with atenolol and bendrofluazide was as effective in reducing blood pressure as the same combination given twice daily, and the hypotensive effect was still present at least 24 hours after the last dose of tablets. A combined tablet of atenolol and bendrofluazide taken once daily would be a simple regimen to follow and would provide almost as much hypotensive effect as a twice-daily regimen incorporating a modest dose of hydrallazine. The hypotensive effect of atenolol was equal to that of bendrofluazide on systolic pressure but significantly better than that of bendrofluazide on diastolic pressure. Atenolol reduced plasma renin and urate concentrations but increased plasma potassium levels. The biochemical effects of atenolol, therefore, may be an advantage over those of bendrofluazide when deciding on first-line treatment for essential hypertension.

Bendroflumethiazide↗
PubMed1976

Clinical pharmacologic observations on atenolol, a beta-adrenoceptor blocker.

The effects of oral and intravenous administration of atenolol were studied in healthy volunteers. The oral administration of a series of single doses of atenolol reduced an exercise tachycardia. After a 200-mg dose, the effect on an exercise tachycardia was maximal at 3 hr and declined linearly with time at a rate of approximately 10% per 24 hr. The peak plasma atenolol concentration occurred at 3 hr and thereafter declined exponentially with time with an elimination half-life of 6.36 +/- 0.55 hr: 43 +/- 3.9% of the dose was excreted in the urine within 72 hr. There was a correlation between the reduction in an exercise tachycardia and the logarithm of the corresponding plasma concentration. The intravenous administration of atenolol reduced exercise tachycardia with a significant correlation between effect and plasma concentration. After 50 mg intravenously, 100% of the dose was recovered from the urine, and the clearance was 97.3 ml/min. Comparison of AUC O leads to chi after oral and intravenous administration of 50 mg showed the bioavailability to be 63% after oral drug. Repeated oral administration of atenolol 200 mg daily either as a single dose or in divided 12 hourly doses for 8 days maintained reduction of an exercise tachycardia of at least 24% during the period of drug administration. The plasma elimination half-life, area under the plasma concentration-time curve, and peak plasma concentration after 200 mg atenolol were not changed by chronic dosing for 8 days.

Administration, Oral↗
PubMed1979

Atenolol and three nonselective beta-blockers in hypertension.

The object of this study was to establish whether cardioselectivity of atenolol confers any advantage over noncardioselective beta-blockade in the treatment of hypertension. A dose of atenolol was established on the basis of morning mean systolic blood pressure (mean of 5 readings) in 27 long-standing hypertensive patients previously controlled on one of three nonselective beta-blockers: propranolol, oxprenolol, or pindolol. Most patients were also taking a diuretic. A crossover trial was then conducted of atenolol and the previous nonselective beta-blocker, each drug being given for 8 wk in randomized order. Other drugs were kept constant. At the end of each 8-wk period a morning test of blood pressure and pulse rate was done, an 11:30 A.M. blood sample was taken for estimation of drug concentration, and spirometry was performed. During the eighth week a glucose tolerance test, fasting lipids, and other biochemical and hematologic estimations were done. On a separate occasion a late morning study was done on the response of blood pressure and pulse rate to three kinds of stress: bicycle ergometer, mental arithmetic, and handgrip. At dosage levels of atenolol giving a mean resting systolic blood pressure equal to that during nonselective beta-blockade, diastolic levels on atenolol tended to be lower at rest and during the mental and handgrip forms of stress. Serum creatinine levels on atenolol were lower than during nonselective beta-blockade. Anti-dioxyribonucleic acid (DNA) titers remained normal in all patients. There was no difference in lung function. There was little difference in glucose and insulin levels during glucose tolerance tests in these patients, half of whom were diabetic. There were no serious side effects but there were a few surprising ones such as vivid dreams in three and muscle cramps in one patient.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Comparison between the acute hemodynamic effects and brain penetration of atenolol and metoprolol.

Atenolol and metoprolol are beta 1-selective adrenergic receptor blockers, devoid of local anesthetic and intrinsic sympathomimetic properties. Their antihypertensive and hypotensive activities are equivalent. They differ with respect to their lipophilic character, as is apparent from their octanol/buffer (pH, 7.4 at 37 degrees C) partition coefficients: metoprolol, 1.084; atenolol, 0.012. We compared the two agents with regard to their acute hemodynamic effects and degree of penetration into the cerebrospinal fluid (CSF) and into the brain. For this purpose [3H]-metoprolol and [14C]-atenolol were injected either intravenously or into the left vertebral artery of chloralose-anesthetized cats. With both routes of administration, metoprolol, the more lipophilic of the two compounds, achieved much higher concentrations in the CSF and in the pontomedullary region than did atenolol. One hour after completion of an intravenous injection, the concentration of metoprolol in the CSF was about 6.5 times higher than that of atenolol; after administration into the vertebral artery, the difference was about ninefold. In spite of these considerable differences, the hypotensive and bradycardic activities of both drugs, administered intravenously or into the left vertebral artery, were virtually the same. These results suggest that the acute hemodynamic effects of metoprolol and atenolol are probably not due to an action within the central nervous system, but rather to a peripheral mechanism.

Animals↗
PubMed1978

Comparative trial of atenolol and propranolol in hyperthyroidism.

1 The use of atenolol, a cardioselective beta-adrenoceptor antagonist, in the management of hyperthyroidism has been studied by comparing it with propranolol. 2 In a double-blind cross-over trial, atenolol (50 mg), propranolol (40 mg) and placebo 4 times daily for 1 week were compared in twenty-one hyperthyroid patients by sequential analysis. 3. Patients generally preferred atenolol or propranolol to placebo but this preference only achieved significance with propranolol. 4 Judged by their effect on the symptoms and signs of hyperthyroidism, both atenolol and propranolol were significantly better than placebo, but no distinction could be made between the two active compounds. 5 Atenolol and propranolol reduced mean heart rate by 29.8 and 27.1% respectively compared with placebo. 6 Atenolol appeared almost equally effective to propranolol in the management of the peripheral manifestations of hyperthyroidism.

Atenolol↗