5-Hydroxytryptamine induces transient Ca 2+ influx through Ni 2+-insensitive Ca 2+ channels in rat vascular smooth muscle cells

Abstract

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