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. 1990 Jun;100(2):370–374. doi: 10.1111/j.1476-5381.1990.tb15811.x

Antagonism by nifedipine of contraction and Ca2(+)-influx evoked by ATP in guinea-pig urinary bladder.

T Katsuragi 1, S Usune 1, T Furukawa 1
PMCID: PMC1917427  PMID: 1696154

Abstract

1. The effects of Ca2(+)-antagonists, especially nifedipine, on contraction and increase of intracellular Ca2+ (Fura-2/AM method) evoked by ATP were evaluated in a thin outer layer segment of guinea-pig urinary bladder. 2. The ATP-evoked contraction was markedly inhibited by dihydropyridine-type Ca2(+)-antagonists, such as nifedipine and nitrendipine, but not by D-600, omega-conotoxin and tetramethrin. 3. This antagonism by nifedipine of ATP-evoked contractions was competitive from the Schild plot analysis, the pA2 value being 8.23. The reduction of ATP-evoked contraction by nifedipine (0.1 microM) was fully reversed by administration of Bay K 8644 (0.1 microM). 4. ATP (100 microM) caused an increase of fluorescence brightness after loading Fura-2/AM, which was coupled with a contraction of the bladder. Both the contraction and the elevation of intracellular Ca2+ evoked evoked by the nucleotide were completely antagonized by nifedipine. by the nucleotide were completely antagonized by nifedipine. 5. These results suggest that ATP may activate the dihydropyridine-sensitive, voltage-dependent Ca2(+)-channels in a direct or indirect fashion and, thereby, elicit a contraction of the bladder.

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Selected References

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