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pubmed:abstractText |
In helical strips of dog cerebral and peripheral arteries, KB-2796 (1-[bis(4-fluorophenyl)-methyl]-4-(2,3,4-trimethoxybenzyl)piperazine dihydrochloride), a new Ca2+ entry blocker, inhibited the contractile responses induced by K+, prostaglandin (PG) F2 alpha and serotonin in a non-competitive manner. KB-2796 inhibited the contraction induced by K+ more effectively than those induced by PGF2 alpha or serotonin. In cerebral arteries, the inhibition produced by KB-2796 was more prominent than in peripheral arteries. In renal arteries, serotonin produced contractions in concentrations 200-1,200 times higher than those sufficient to contract the other arteries. KB-2796 inhibited renal arterial contractions induced by serotonin and K+ to a similar extent. In renal arteries depolarized by replacement of the entire amount of NaCl in the bathing medium with KCl, PGF2 alpha produced additional contraction of the artery, whereas serotonin did not contract the artery. These results suggest that KB-2796 inhibits the contractility of cerebroarterial smooth muscle more preferentially than that of other arteries. The contractile response to serotonin of the renal artery appears to be associated with the voltage-dependent influx of Ca2+ as suggested in the cerebral arteries.
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