It has been known that calcium antagonists also inhibit the radioligand binding to muscarinic and $alpha$-adrenergic receptors and, in case of verapamil, these inhibitions may play a role in the effects of verapamil on the heart. In this study, the effects of nicardipine, nifedipine, nimodipine, diltiazem and verapamil on the binding of [$^3H$]dihydroalprenolol (DHA) to dog cardiac ${eta}$-adrenergic receptors were examined. A single uniform [$^3H$]DHA binding site ($K_D/= 5nM;and;B_{max}=2600$ fmol/mg protein) was identified in dog cardiac sarcolemma. [$^3H$]DHA binding was not affected by the usual therapeutic concentrations of these calcium antagonists (nanomolar range) but in the "nonspecific"concentration ranges ($28-180{mu}m$) these drugs inhibited [$^3H$]DHA binding to $eta$-adrenergic receptors. Nicardipine, nifedipine, nimodipine and diltiazem competed for [$^3H$]DHA binding to ${eta}$-adrenergic receptors with dissociation constants ($K_i$) of $28{mu}m,' 74{mu}m, 39{mu}m ;and ;35{mu}m,$ respectively. Verapamil ($K_i=176.5 {mu}m$) was less potent inhibitor than other drugs and this inhibition was noncompetitive; the maximal binding capacity ($B_{max}$) $300 {mu}m$ verapamil without change in the apparent dissociation constant (4K_D$) for DHA. These results indicate that the inhibitory action of calcium antagonists at high concentrations on ${eta}$-adrenergic receptors is not involved in the therapeutic effects of these drugs by the calcium channel blocking action.