The isothiocyanate analog (IBI) of tolazoline produced contraction of the rat aortic strip, with an ED<sub>50</sub> value of 1.63 × 10<sup>–5</sup> M. The maximum contraction of the analog was nearly equal to that of tolazoline or phenylephrine. At 27 °C the tissue reactivity of phenylephrine and IBI was similar. When compared at equiactive concentrations, the total duration of contraction of IBI was three times longer than that of tolazoline. Thus, the longer duration of action of IBI may be attributed to the S=C=N group substitution of the molecule. IBI at 10<sup>-6</sup> M shifted the dose-response curve of phenylephrine to the right with reduction in maxima. Phentolamine and other α<sub>1</sub>or α<sub>2</sub> adrenoceptor blockers failed to block the responses of IBI in aorta, whereas verapamil or nifedipine blocked the response significantly. It appears that IBI is acting through calcium-channel-sensitive or calcium-receptor-related mechanism(s). In aspirin-treated platelets from human plasma, a distinct phase of aggregation induced by epinephrine can be blocked by IBI with KB of 2 × 10<sup>–5</sup> M. This indicates a small but selective α<sub>2</sub> related action of IBI. The aggregation induced by ADP or second component of aggregation induced by epinephrine were also blocked by IBI at concentrations comparable to that of the 012-adrenoceptor-mediated response. This indicates a lack of specificity of IBI in differentiating various phases of aggregation. Therefore, as compared to tolazoline, IBI presents an interesting paradox in its interaction with various receptors or mechanisms in the vascular tissue and platelets.