Utilizing the whole-cell patch-clamp method we assessed the Ca2+ current (ICa) 
in well-established cell lines from human small-cell carcinoma (SCC) of the 
lung, NCI-H209 and NCI-H187. The Ca2+ current was readily observed in H209 
tumour cells (90% of the cells tested), whereas H187 tumour cells only 
occasionally expressed Ca2+ channels (26% of the cells tested). H209 Ca2+ 
current was evoked by potentials greater than -30 mV and exhibited partial 
inactivation over the duration of a 40 ms command potential. This inward current 
was unchanged by alteration of the holding potential from -80 to -40 mV and the 
activation phase of the Ca2+ current was best fitted by Hodgkin-Huxley m(t)2 
kinetics. H209 Ca2+ current was reduced over 80% by verapamil (100 microM), 
whereas w-conotoxin (5 microM) appeared to be without effect. In contrast, H209 
Ca2+ current was rapidly abolished by nifedipine (10 microM), strongly 
suggesting the presence of L-type Ca2+ channels. Voltage-gated Ca2+ channels may 
be important to the secretion of ectopic hormones and the etiology and 
pathogenesis of Lambert-Eaton syndrome, an autoimmune disorder of the motor 
nerve terminal in which autoantibodies directed against voltage-gated Ca2+ 
channels are produced.