5-hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitiveCa2+ channels in rat vascular smooth muscle cells

The effects of Ni2+, a non-selective cation channel inhibitor, on 5-hydroxy tryptamine (5-HT)- and angiotensin II (Ang II)-induced intracellular Ca2+ d ynamics in rat aortic smooth muscle cells were investigated. Ni2+ (1 mM) si gnificantly inhibited the transient increase in intracellular Ca2+ concentr ation ([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 inc rease in Ca2+ influx induced by 5-HT (10 mu M), while significantly suppres sed the sustained increase. Ca2+ influx evoked by high KCl (80 mM), thapsig argin (TG) (1 mu M) or depletion of intracellular Ca2+ store was almost com pletely suppressed by Ni2+. Ni2+ had no effect on 5-HT-induced inositol tri phosphate production and Ca2+ release from the intracellular store(s). Thes e 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. (C) 1999 Elsevier Scienc e B.V. All rights reserved.