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

General Pharmacology
M HashimotoS Shibata

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 ...Continue Reading

References

May 1, 1985·Journal of Cardiovascular Pharmacology·M SchrammG Thomas
Jul 20, 1984·European Journal of Pharmacology·H YamamotoC Van Breemen
Nov 1, 1984·Canadian Journal of Physiology and Pharmacology·C M SuD J Triggle
Jan 16, 1981·European Journal of Pharmacology·R Towart, E Perzborn

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