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• W1979622576 abstract "The effects of Bay K 8644 on the reactivity and 45Ca2+ uptake in segments from human cerebral arteries were studied. Bay K 8644 induced concentration-dependent contractions up to 10−6 M; 10−5 M produced a reduction of the maximal response. The Ca2+ agonist elicited these contractions by itself, and no previous depolarization was needed. The response to Bay K 8644 was antagonized competitively by nifedipine (5 × 10−8 and 10−7 M, πA2 value of 8.17) and non-competitively by verapamil (10−6, 5 × 10−6 and 10−5 M). The contraction induced by 10−7 M Bay K 8644 was inhibited by a Ca2+-free medium containing 1 mM EGTA. The subsequent cumulative Ca2+ addition, caused concentration-dependent contractions up to 2.5 mM Ca2+, which were reduced by nifedipine (10−8 and 10−7 M) or verapamil (5 × 10−6 and 10−5 M). When the EGTA concentration in the Ca2+-free solution was reduced to 0.1 mM, contractions induced by Ca2+ up to 5 mM, including 0 Ca2+, were increased with respect to those obtained in the presence of 1 mM EGTA. Basal 45Ca2+ uptake was not modified with Bay K 8644 (10−6 M) or nifedipine (10−6 M). K+ (25 and 50 mM) produced an increase on 45Ca2+ uptake, which was potentiated by Bay K 8644 (10−6 M) and antagonized by nifedipine (10−6 M); this latter agent reduced the potentiation elicited by the Ca2+ agonist. These results suggest that contractions caused by Bay K 8644 in human cerebral arteries are produced by the opening of the voltage-dependent Ca2+ channels present in vascular smooth muscle cells, which appear to be preactivated in a basal situation, facilitating Ca2+ influx. Nevertheless, Bay K 8644 needed a previous cell depolarization to produce an increase in 45Ca2+ uptake." @default.
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• W1979622576 date "1989-06-01" @default.
• W1979622576 modified "2023-10-17" @default.
• W1979622576 title "Vasoconstrictor effect of the Ca2+ agonist Bay K 8644 on human cerebral arteries" @default.
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• W1979622576 doi "https://doi.org/10.1016/0006-8993(89)90438-1" @default.
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