Potentiating effect of Bay K 8644 on the noradrenaline-induced contraction in rabbit renal and femoral arteries

Abstract

1. In rabbit renal and femoral arteries, Bay K 8644 produced a contraction and nifedipine inhibited it. 2. Bay K 8644 potentiated the responses to noradrenaline (NA) and potassium (K+). In the presence of nifedipine, Bay K 8644 potentiated NA. 3. In a Ca2+-free medium with EGTA, NA produced a transient contraction which was not affected by Bay K 8644 or nifedipine. Bay K 8644 enhanced the Ca2+-induced contraction in a Ca2+-free medium containing EGTA, nifedipine and NA. 4. The combined treatment with nimodipine and nifedipine further inhibited the Bay K 8644 induced potentiation of Ca2+ responses in the presence of NA as compared to nifedipine alone. 5. In the presence of but not absence of Bay K 8644, Ca2+ caused contractions in a Ca2+-free medium containing EGTA, nifedipine and KCl. 6. Vanadate further enhanced the Bay K 8644 induced potentiation of the Ca2+ responses in the presence of K+ but not NA. 7. These results suggest that, in rabbit renal and femoral arteries, Bay K 8644 does not affect the intracellular translocation of Ca2+ but increases Ca2+-influx activated by K+ or NA. Bay K 8644-induced potentiation of NA responses is likely due to an increase in Ca2+-influx through voltage operated channels (VOC) activated by NA. Also, K+ activated VOC may be coupled to Ca2+-extrusion pumps more than NA activated VOC.