Key result
Infusion of atenolol, metoprolol, timolol, and propranolol significantly inhibited norepinephrine-induced cardiac responses in isolated rat hearts, whereas bolus injections of atenolol, metoprolol, and timolol were ineffective.
Atenolol displays a different time course of action on NE-induced cardiac responses depending on administration route (bolus vs infusion), likely due to its low lipophilicity.
May warrant caution with bolus dosing of hydrophilic beta-blockers; leaves open route-dependent effects for clinical validation.
The effects of atenolol and another three beta-adrenoceptor blocking agents on norepinephrine (NE)-induced cardiac responses were examined in isolated and perfused rat hearts following a Langendorff method. Bolus injection of atenolol did not show significant inhibitory effects on NE-induced increases in myocardial contractile force (MCF) and heart rate. Bolus injections of metoprolol and timolol were also ineffective for inhibiting NE-responses. However, both bolus injection and infusion of propranolol or infusion of atenolol, metoprolol and timolol all significantly inhibited NE-responses. On sustained increase in MCF induced by infusion of NE, the inhibitory effect of atenolol was transient, while that of propranolol was continuous. From these results, it is concluded that atenolol displays a different time course of action on NE-induced cardiac responses by bolus injection or infusion because of its pharmacological properties, which may be due to its low lipophilicity.
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Nakasone et al. (1988) studied this question. Atenolol, metoprolol, timolol, and propranolol was evaluated on Norepinephrine (NE)-induced increases in myocardial contractile force (MCF) and heart rate. Infusion of atenolol, metoprolol, timolol, and propranolol significantly inhibited norepinephrine-induced cardiac responses in isolated rat hearts, whereas bolus injections of atenolol, metoprolol, and timolol were ineffective.
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