The β-Adrenergic Blockade Withdrawal Phenomenon

Chronic β1‐adrenoceptor antagonist treatment sensitizes β2‐adrenoceptors, but desensitizes M2‐muscarinic receptors in the human right atrium

“…Firstly, when muscarinic receptor function decreases, the inhibitory influence of the vagus on cardiac 6-adrenoceptor function is attenuated. Thus, such a reduction in vagal activity might exaggerate the symptoms of adrenergic hypersensitivity often observed after abrupt withdrawal of f6-adrenoceptor antagonist treatment in patients suffering from hypertension or angina pectoris (Prichard et al, 1983). Such withdrawal phenomena that were initially observed after sudden cessation of propranolol treatment (Prichard et al, 1983) can also occur after sudden withdrawal of l1-adrenoceptor antagonists : Walden et al (1988) have recently shown, in healthy volunteers, that abrupt withdrawal of atenolol markedly increases the sensitivity of human cardiac fi-adrenoceptors to isoprenalineinduced tachycardia, but not to exercise-induced tachycardia.…”

“…Thus, such a reduction in vagal activity might exaggerate the symptoms of adrenergic hypersensitivity often observed after abrupt withdrawal of f6-adrenoceptor antagonist treatment in patients suffering from hypertension or angina pectoris (Prichard et al, 1983). Such withdrawal phenomena that were initially observed after sudden cessation of propranolol treatment (Prichard et al, 1983) can also occur after sudden withdrawal of l1-adrenoceptor antagonists : Walden et al (1988) have recently shown, in healthy volunteers, that abrupt withdrawal of atenolol markedly increases the sensitivity of human cardiac fi-adrenoceptors to isoprenalineinduced tachycardia, but not to exercise-induced tachycardia. Isoprenaline-induced tachycardia is a mixed cardiac fl-and f2-adrenoceptor-mediated effect, while exercise-induced tachycardia is a pure l1-adrenoceptor-mediated effect McDevitt, 1989;Motomura et al, 1990).…”

Antianginal Actions of Beta-Adrenoceptor Antagonists

“…Exacerbations of angina, myocardial infarction, and increased risk of sudden death have been reported following abrupt cessation of b-adrenoceptor antagonists after longterm therapy; 24 therefore, patients should be warned against interruption or discontinuation of b-adrenoceptor antagonists without the advice of their physician. The mechanism underlying this phenomenon is not completely understood, but may involve increased sensitivity to b-adrenoceptor agonists and an upregulation in the number of b-adrenoceptors when the antagonist is abruptly withdrawn.…”

Letter by Poullis Regarding Article, “Efficacy of Long-Term β-Blocker Therapy for Secondary Prevention of Long-Term Outcomes After Coronary Artery Bypass Grafting Surgery”

“…2 Of note, a very high incidence of elective work (98%) formed the study cohort. Currently, 10% to 20% of isolated coronary artery bypass graft cases in the United Kingdom are urgent, 3 with a higher rate in the United States.…”