Propranolol in Patients with Angina Pectoris

Gianelly, Ralph E.; Goldman, Robert H.; Treister, Bernard; Harrison, Donald C.

doi:10.7326/0003-4819-67-6-1216

Cited by 109 publications

(27 citation statements)

References 18 publications

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“…However, it is interesting to note that the orthostatic change in heart rate transiently increased more than threefold between 24 and 48 h after the last dose. It is unlikely that these experimental and clinical findings can be attributed merely to an increase in catecholamine levels during withdrawal since acute increases in plasma or urinary catecholamines have not been seen following abrupt withdrawal of either propranolol or metoprolol (13,(47)(48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.

Aarons¹,

Nies²,

Gál³

et al. 1980

J. Clin. Invest.

288

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A B S T R A C T Abrupt withdrawal after the chronic administration of propranolol has resulted in clinical syndromes that suggest adrenergic hypersensitivity. The effect of propranolol administration and withdrawal on ,-adrenergic receptors was studied in human lymphocyte membranes. Receptor density was quantitated by direct binding assays with the radioligand [1251]iodohydroxybenzylpindolol. Administration ofpropranolol (160 mg/d) for 8 d resulted in trough plasma levels of -35 ng/ml. By day 5 ofpropranolol administration the density of /3-adrenergic receptors had increased 43+4% (P < 0.01) above pretreatment levels. Abrupt withdrawal of propranolol was followed by the disappearance of propranolol from the plasma within 24 h. The density of f3-adrenergic receptors did not return to pretreatment level for several days. Physiologic supersensitivity of 8-adrenergic receptor-mediated responses was suggested by the appearance of significant increases in the orthostatic change in heart rate (P < 0.05) and the orthostatic change in the heart rate-systolic blood pressure product (P < 0.01) during the first 48 h after propranolol withdrawal. These data show that propranolol administration leads to an increase in the density of f3-adrenergic receptors in human tissue. The results are consistent with the hypothesis that some of the untoward effects observed after abrupt discontinuation of propranolol are caused by 8-receptor-mediated adrenergic hypersensitivity.

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Section: Discussionmentioning

confidence: 99%

Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.

Aarons¹,

Nies²,

Gál³

et al. 1980

J. Clin. Invest.

288

View full text Add to dashboard Cite

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“….3adrenergic receptor blocking agents have addded a new dimension to the medical management of patients with stable angina pectoris (Amsterdam, Gorlin & Wolfson, 1969;Hamer & Sowton, 1966;Gianelly et al, 1967). However, unwanted and potentially hazardous side effects have been documented in as many as 10% of patients (Greenblatt & Koch-Weser, 1974).…”

Section: Introduction Methodsmentioning

confidence: 99%

The combination of nifedipine and propranolol in the management of patients with angina pectoris.

Tweddel¹,

Beattie²,

Murray³

et al. 1981

Brit J Clinical Pharma

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1 A double‐blind cross over study was carried out to assess the effects of the combination of nifedipine and propranolol in 25 patients with chronic stable angina pectoris at beta‐adrenoceptor blockade. 2 Efficacy was judged objectively by a standardized exercise protocol using a bicycle ergometer and subjectively by patient assessment of anginal attack rate. 3 The combination of nifedipine and propranolol was shown to be effective with an increase in exercise time to angina and an increase in physical work capacity expressed in terms of calculated maximal oxygen uptake (VO2 max). There was an associated reduction in anginal attack rate. 4 The synergistic effect was even more pronounced after reduction in propranolol dosage to 50% of the beta‐adrenoceptor blocking dose, reflecting the myocardial depressant effects of beta‐adrenoceptor blocking drugs in these patients with coronary heart disease, some of whom had poor left ventricular function.

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“…It is for these reasons that pharmacological measures to interfere with this activity first seemed a logical approach to the treatment of angina.2 Propranolol, an effective beta-adrenergic receptor-blocking drug, represents one such potential therapeutic agent, and the conclusions of several studies have suggested its efficacy. [3][4][5][6][7] Evaluation of drugs in angina pectoris has been imperfect because subjective improvement in response to therapy is difficult to estimate in this disease, and objective methods of testing have often not been adequately performed. It is possible, however, to establish a standardized exercise testing program using the treadmill wherein the variability in level of exercise necessary to produce angina can be minimized.…”

mentioning

confidence: 99%

Effects of Propranolol and Isosorbide Dinitrate on Exercise Performance and Adrenergic Activity in Patients with Angina Pectoris

1969

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SUMMARYTwelve patients with angina pectoris were evaluated in a single blind crossover study with respect to objective changes in exercise performance on the treadmill and subjective, clinical improvement on oral administration of propranolol, isosorbide dinitrate (ISD), and a combination of propranolol and ISD. Combined objective and subjective evaluations showed that nine of 12 patients improved on propranolol, seven of 10 on ISD, and all 10 on the combination of drugs. The differences in objective improvement between the various drug regimens were not significant. However, subjectively all patients on the combination of drugs improved markedly. The patients on propranolol or the combination had a decrease in pressure-rate index of about 30% both at rest and during exercise, while these values did not change on ISD. A significant reduction in exercise-induced S-T depression was observed with propranolol alone and in combination with ISD at grade 3+ pain. Adrenergic activity, estimated from plasma and urinary catecholamines, appeared to be increased in these patients before drug treatment and was not altered during treatment. It is concluded that propranolol, ISD, and the combination of these drugs all improve exercise performance in patients with angina. Although the combination of drugs could not be shown to produce a greater increase in exercise performance than either drug alone, the combination effected a greater overall clinical improvement. Additional

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Propranolol in Patients with Angina Pectoris

Cited by 109 publications

References 18 publications

Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.

Elevation of beta-adrenergic receptor density in human lymphocytes after propranolol administration.

The combination of nifedipine and propranolol in the management of patients with angina pectoris.

Effects of Propranolol and Isosorbide Dinitrate on Exercise Performance and Adrenergic Activity in Patients with Angina Pectoris

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