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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Calcium antagonism by KB-2796, a new diphenylpiperazine analogue, in dog vascular smooth muscle.

The effects of KB-2796, a new diphenylpiperazine analogue, on [3H]nitrendipine ([3H]NTD) binding, KCl-induced contraction and 45Ca influx has been examined in dog vascular smooth muscle, and compared with those of other diphenylpiperazines. In the binding study, [3H]NTD was found to bind with a high affinity to a single class of sites on aortic membranes (Kd = 0.41 nM and Bmax = 31 fmol (mg protein)-1). KB-2796 inhibited specific [3H]NTD binding in a concentration-dependent manner, with a Ki value of 0.34 microM. The other diphenylpiperazine derivatives such as flunarizine and cinnarizine also inhibited binding in the same manner. Also, in the contraction study, all the diphenylpiperazines antagonized the 50 mM KCl-induced contraction of isolated mesenteric arteries concentration-dependently. The IC50 values of the compounds for KCl-induced contraction correlated strongly with the respective Ki values obtained in the [3H]NTD binding study. In the 45Ca influx study, KB-2796 also effectively inhibited KCl-induced 45Ca influx in mesenteric arteries, with an IC50 value of 0.14 microM. This was close to the IC50 value found in the KCl-induced contraction study. These findings suggest that calcium antagonism by KB-2796 is responsible for its vasorelaxing action in vascular smooth muscle.[1]

References

  1. Calcium antagonism by KB-2796, a new diphenylpiperazine analogue, in dog vascular smooth muscle. Iwamoto, T., Morita, T., Sukamoto, T. J. Pharm. Pharmacol. (1991) [Pubmed]
 
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