Nifedipine-activated Ca 2ϩ permeability in newborn rat cortical collecting duct cells in primary culture. Am J Physiol Cell Physiol 280: C1193-C1203, 2001.-To characterize Ca 2ϩ transport in newborn rat cortical collecting duct (CCD) cells, we used nifedipine, which in adult rat distal tubules inhibits the intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) increase in response to hormonal activation. We found that the dihydro-pyridine (DHP) nifedipine (20 M) produced an increase in [Ca 2ϩ ]i from 87.6 Ϯ 3.3 nM to 389.9 Ϯ 29.0 nM in 65% of the cells. Similar effects of other DHP (BAY K 8644, isradipine) were also observed. Conversely, DHPs did not induce any increase in [Ca 2ϩ ]i in cells obtained from proximal convo-luted tubule. In CCD cells, neither verapamil nor diltiazem induced any rise in [Ca 2ϩ ]i. Experiments in the presence of EGTA showed that external Ca 2ϩ was required for the nifed-ipine effect, while lanthanum (20 M), gadolinium (100 M), and diltiazem (20 M) inhibited the effect. Experiments done in the presence of valinomycin resulted in the same nifedi-pine effect, showing that K ϩ channels were not involved in the nifedipine-induced [Ca 2ϩ ]i rise. H2O2 also triggered [Ca 2ϩ ]i rise. However, nifedipine-induced [Ca 2ϩ ]i increase was not affected by protamine. In conclusion, the present results indicate that 1) primary cultures of cells from terminal nephron of newborn rats are a useful tool for investigating Ca 2ϩ transport mechanisms during growth, and 2) newborn rat CCD cells in primary culture exhibit a new apical nifedipine-activated Ca 2ϩ channel of capacitive type (either transient receptor potential or leak channel).