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  • Title: The effects of BAY-K-8644 on the contraction of cat middle cerebral and femoral arteries.
    Author: Salaices M, Marin J, Sanchez-Ferrer CF, Reviriego J.
    Journal: Biochem Pharmacol; 1985 Sep 01; 34(17):3131-5. PubMed ID: 2412563.
    Abstract:
    The effects of BAY-K-8644 on the reactivity of cylindrical segments of cat middle cerebral and femoral arteries were studied. BAY-K-8644 induced dose-dependent contractile responses in cerebral arteries up to 10(-6) M; higher concentrations tended to cause relaxation of the segments. The dihydropyridine elicited contractions in femoral arteries only when these vessels were previously exposed to 15 mM K+. Nifedipine (3 X 10(-7) M) produced a parallel shift to the right of the dose-response curve to BAY-K-8644, whereas 5 X 10(-6)M verapamil markedly reduced the responses evoked by all concentrations of this drug. The removal of Ca2+ from the medium abolished the response evoked by the Ca2+-channel activator at 10(-7) M in both kinds of arteries. Under these conditions Ca2+ addition induced vasoconstriction, which was blocked by nifedipine (3 X 10(-7) M). Preincubation of femoral arteries with 10(-7) M BAY-K-8644 potentiated the effects evoked by 25, 50, 75 and 125 mM K+, but did not modify those produced by 10(-5) M noradrenaline. Nifedipine (10(-7) M and 3 X 10(-7) M) blocked the potentiation caused by this drug in a dose-dependent manner. Both the increase of the response elicited by BAY-K-8644 and the inhibitory effects of nifedipine were greater at 25 mM K+ than at 125 mM. These results suggest that BAY-K-8644 facilitates Ca2+ influx into smooth muscle through Ca2+ channels that are possibly voltage sensitive and the voltage independence of the drug-induced contractions in cerebral arteries.
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