Intracellular [Ca+ + ]i was examined using Quin-2. Resting [Ca+ + ]i in platelets loaded with Quin-2 in media containing either 1 mmol/L CaCl2. or 2 mmol/L EGTA was 52.1?5.2nmol/L, 28.4+5.1 nmol/L, respectively. The concentration of external calcium appears to play an important role in cytosolic Cat++ hemeostasis in platelets. Stimulation with A2 3187( 25nmol/L ) caused [Ca++]i to peak at 145?30.8 nmol/L in the presense of extracellular 1mmol/L CaCl2 and 34.4?2.4 nmol/L after addition of 2 mmol/L EGTA. These data suggested that the most of this rise results from calcium entry across the plasma membrane, with a small contribution to the discharge of intracellular pool of Ca++.Anisodamine ( 100?mol/L ) had no effects on resting [Ca + + ]i and A23187-evoked [Ca++]i level in the absence of CaCl2, Anisodamine ( 100?mol/L, 25?mol/L), verapamil ( 10?mol/L ) decreased the A23187 -evoked [Ca++ ]i rises in the presence of CaCl2 by 38%, 34%, 25%, respectively. These results provided a mechanism for the calcium antagonistic effects of Anisodamine.