5-hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells.

摘要

The effects of Ni2+, a non-selective cation channel inhibitor, on 5-hydroxytryptamine (5-HT)- and angiotensin II (Ang II)-induced intracellular Ca2+ dynamics in rat aortic smooth muscle cells were investigated. Ni2+ (1 mM) significantly inhibited the transient increase in intracellular Ca2+ concentration ([Ca2+]i) induced by Ang II (100 nM) in aortic smooth muscle cells, as measured using fura-2. However, Ni2+ did not suppress the transient increase in Ca2+ influx induced by 5-HT (10 microM), while significantly suppressed the sustained increase. Ca2+ influx evoked by high KCl (80 mM), thapsigargin (TG) (1 microM) or depletion of intracellular Ca2+ store was almost completely suppressed by Ni2+. Ni2+ had no effect on 5-HT-induced inositol triphosphate production and Ca2+ release from the intracellular store(s). These results suggest that 5-HT, but not Ang II, induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels, which are distinguishable from the voltage-dependent or store-operated Ca2+ channels.