Comparative study of store-operated channels and the effects of nitric oxide on capacitative Ca2+ influx in platelets, smooth muscle cells, and jurkat T-lymphocytes

Recently we have described small (3 pS) conductance nonselective cation channels in vascular smooth muscle cells (SMC) that are activated by depletion of intracellular Ca2+ stores in intact cells. These channels can be also activated in excised membrane patches by the Ca2+ influx factor (CIF) partially purified from human platelets. Store-operated nonselective cation channels have the properties that distinguish them from highly Ca2+-selective Ca2+ release-activated Ca2+ (CRAC) channels known to mediate capacitative Ca2+ influx in Jurkat T-lymphocytes and some other nonexcitable cells. Here we show that depletion of Ca2+ stores in human platelets causes activation of small conductance (2.6 pS) nonselective cation channels that resemble the store-operated nonselective cation channels in SMC, and are different from Ca2+-selective CRAC channels described in Jurkat cells. Previously we demonstrated that nitric oxide (NO) inhibits store-operated cation influx in human platelets and SMC by accelerating sarcoplasmic-endoplasmic reticulum Ca2+-ATPase [SERCA]-dependent refilling of Ca2+ stores. Here we present evidence that Ca2+ influx in Jurkat cells could also be inhibited by NO as a result of enhanced refilling of intracellular stores, although this effect could be masked if agonist-induced Ca2+ release significantly exceeds Ca2+ re-uptake into the stores. Thus, by promoting the refilling of intracellular Ca2+ stores NO can inhibit store-operated Ca2+ influx mediated either by nonselective cation channels or by CRAC channels.