Calcium influx by hypertonicity through the voltage-dependent calcium channels

Abstract

We found out before the facts that propylene glycol (PG) raises the intracellular calcium concentration ([Ca2+]i) and that hypertonicity induced by PG is involved in the [Ca2+]i rise. The present study was conducted for the purpose of determining whether the Ca2+ influx through the Ca2+ channels is related to the rise in [Ca2+]i incuded by hypertonicity. A Ca2+-free saline and all of the Ca2+ channel blockers CdCl2 (0.1 mM), o-conotoxin GVIA (1 µM), verapamil (10 µM), and nicardipine (10 µM) significantly decreased the [Ca2+]i raised by hypertonicity. Bay K 8644 (4 µM), a Ca2+ channel activator, potentially increased the [Ca2+]i raised by hypertonic salines. The results described above lead me to the conclusion that the Ca2+ influx through the voltage-dependent Ca2+ channels is involved in the hypertonicity-induced [Ca2+]i rise.