AbstractWe have previously reported the presence, in Jurkat T cells, of outward K+currents and inward currents that have been attributed to Ca2+channels. Here, we have studied the effects of dimethyl 1,4‐dihydro‐ 2,6‐dimethyl‐4‐(2‐nitrophenyl)‐3,5‐pyridine‐dicarboxylate (nifedipine) and 4‐(2,l,3‐benzoxadiazol‐4‐yl)‐l,4‐dihydro‐ 2,6‐dimethyl‐5‐methoxy‐carbonylpyridine‐3‐carboxylate (PN200‐110), two dihydropyridines (DHPs) known to inhibit voltage‐dependent Ca2+channel activity in different types of cells, and two inhibitors of internal Ca2+release (muscle cells), ryanodine and 3,4,5‐trimethoxybenzoic acid 8‐(diethylamino)octyl ester (TMB‐8), on thePhaseo‐ lus vulgarisphytohemagglutinin (PHA)‐dependent responses in Jurkat T lymphocytes. Our results show that nifedipine and PN200‐110 inhibit the PHA‐dependent production of interleukin‐2 except when 12‐0‐ tetradecanoyl‐13‐O‐acetyl phorbol is added to the cultures. Ryanodine and TMB‐8 are not inhibitors. The PHA‐dependent Ca2+response is significantly reduced when the cells are preincubated in the presence of the DHPs. Under these conditions, ryanodine has only a small inhibitory effect and TMB‐8 has no effect. In contrast, only ryanodine (50μM) decreases the PHA‐ dependent cytosolic release of Ca2+when the cells are bathed in a medium containing a low concentration of Ca2+(60 nM). The inhibitory effects of nifedipine and PN200‐110 may result from the binding of these DHPs to specific receptor sites as revealed by studies using [3H]PN200‐110 (KD ‐ 8.5 ± 3.1 nM; 2300 ± 500 apparent binding sites/cell). Photoaffinity labeling studies using [3H]azidopine as a probe showed specific incorporation of label into three glycoproteins of molecular mass (± SD) 170 ± 13, 110 ± 25, and 60 ± 17 kd as analyzed by electrophoresis under reducing conditions.