Inhibitors of inositol trisphosphate-induced Ca 2+ release from isolated platelet membrane vesicles
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 36, Issue: 20, Page: 3331-3337
1987
- 40Citations
- 7Captures
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Metrics Details
- Citations40
- Citation Indexes40
- 40
- CrossRef31
- Captures7
- Readers7
Article Description
Platelet membrane vesicles accumulated Ca 2+ in an ATP-dependent fashion, and 25–50% of the accumulated Ca 2+ was released by the addition of 10 μM inositol 1,4,5-trisphosphate (IP 3 ). The concentration of IP 3 required for half-maximal Ca 2+ release was approximately 0.5 μm. The inhibition of IP 3 -induced Ca 2+ release from these membrane vesicles by various agents was examined. Of the plasma membrane Ca 2+ channel blockers, cinnarizine and flunarizine were found to be potent inhibitors of IP 3 -induced Ca 2+ release while having no effect on ATP-dependent Ca 2+ uptake. The ic 50 value for both cinnarizine and flunarizine as inhibitors of IP 3 -induced Ca 2+ release was below 10 −6 M. Nifedipine, verapamil, bepridil, and diltiazem did not significantly inhibit IP 3 -induced Ca 2+ release at the highest concentration tested (50 μM). The “intracellular Ca 2+ antagonists” ryanodine, TMB-8 (8-( N, N -diethylamino)octyl-3,4,5-trimethoxybenzo dantroline, trifluoperazine and chlorpromazine were not inhibitors of IP 3 -induced Ca 2+ release at 50 μM. The local anesthetics benzocaine and lidocaine weakly inhibited the IP 3 -induced Ca 2+ release with ic 50 values of approximately 5 and 50 μM, respectively, whereas other local anesthetics tested were less potent inhibitors. The potent inhibitors described may prove useful as probes of the IP 3 -induced Ca 2+ release channels.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0006295287903078; http://dx.doi.org/10.1016/0006-2952(87)90307-8; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023484753&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/3499904; https://linkinghub.elsevier.com/retrieve/pii/0006295287903078; http://dx.doi.org/10.1016/0006-2952%2887%2990307-8; https://dx.doi.org/10.1016/0006-2952%2887%2990307-8
Elsevier BV
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