We studied interactions between the putative calcium entry promotor Bay k 8644 and alpha 1-adrenoceptor-mediated increases in diastolic pressure elicited by cirazoline as well as alpha 2-adrenoceptor-mediated pressor responses induced by B-HT 920 in pithed cats. Bay k 8644 (0.01-1 mg/kg, i.a.) did not affect the log dose-pressor response curve of cirazoline, but slightly potentiated the increase in diastolic pressure elicited by B-HT 920. After attenuation of the B-HT 920-induced pressor effects by the calcium entry blocker nifedipine (0.1 mg/kg, i.a.), Bay k 8644 (0.1 mg/kg, i.a.) strongly enhanced the pressor response. The increase in diastolic pressure elicited by cirazoline was not affected by nifedipine (0.1 mg/kg, i.a.), and the addition of Bay k 8644 (0.1 mg/kg, i.a.) had no effect. We conclude that in contrast to the increase in diastolic pressure elicited by B-HT 920, calcium channels are not involved in the cirazoline-induced pressor responses in the pithed cat. The activation of the calcium channels by B-HT 920 is already so efficient that it cannot be further enhanced by Bay k 8644.