Why does depolarisation by high intracellular K+ trigger calcium channels opening?
Ca2+ is very often the trigger to release neurotransmitter or, in this case, hormones. Ca2+ entry in the cell is important to activate the fusion of secretory vesicles with the membrane in pancreatic beta cells as shown in Fig. 1 (Thurmond, 2000). The function of Ca2+ entry is not so much related to its depolarizing actions.


Fig. 1. Ca2+-mediated insulin secretion. Glucose-stimulates insulin secretion by increasing the ATP/ADP ratio, which inhibits the ATP-sensitive KATP-channels, leading to membrane depolarization and opening of voltage-dependent calcium channels (VDCC), with a resultant major increase in cytosolic calcium, which, in turn, triggers exocytosis. SNARE proteins play a critical role in insulin granule secretion. The linking of the plasma membrane proteins syntaxin and SNAP-25 to vesicle protein VAMP-2/synaptobrevin-2 cause the docking of the vesicle, bringing insulin granules in close contact with the plasma membrane and calcium channels, after opening of calcium channels, the readily releasable pool (RRP) insulin granules located nearby are exposed to high level of Ca2+, resulting in RRP granule exocytosis. Source: Ren et al. (2007) 

Ca2+ entry in the cell is potentially toxic and closely regulated. For example, internal stores are actively involved in the release and re-uptake of Ca2+ (Pian-Smith et al., 1988). Although Ca2+ influx will depolarize the cell further, it will not contribute substantially to the membrane potential compared to the effects of K+ and Na+. 

References
- Pian-Smith et al., Endocrinology (1988); 123(4):1984-91
- Ren et al.,  J Transl Med (2007)
- Thurmond, Landes Bioscience (2000)