Effects of Bay K 8644 on 45Ca Uptake and Efflux and on Contraction in the Rabbit Aorta

Contractions induced by K+, noradrenaline and 11,9-epoxymethano prostaglandin H2 (11,9-epoxymethano PGH2) were accompanied by a large, moderate and negligible stimulation of 45Ca uptake in rabbit aortic rings, respectively. Bay K 8644, 14 and 56 nM, enhanced both the contraction and the 45Ca uptake stimulated by all 3 agonists. In the absence of agonists, Bay K 8644 (14 and 56 nM) caused a small contraction and increase in 45Ca uptake. 45Ca efflux was increased by noradrenaline, and Bay K 8644 augmented this. In Ca-free solution, contractions induced by noradrenaline or 11,9-epoxymethano PGH2 were not augmented by Bay K 8644. Nifedipine (0.1 microM) antagonized 45Ca uptake stimulated by K+ or noradrenaline. Nifedipine also reduced the stimulant effect of Bay K 8644 on 45Ca uptake in the presence of all three agonists. It is concluded that, in the rabbit aorta, Bay K 8644 enhances the opening of Ca channels both during depolarization and in the presence of receptor-specific agonists and is also able to open Ca channels under basal conditions. Bay K 8644 appears not to reduce Ca efflux or enhance Ca release from intracellular stores.