Nifedipine induced modulations of intrathyroidal radioiodine turnover kinetics has been studied in euthyroid and thyrotoxicosis individuals. Nifedipine has been found to suppress Amax significantly (p < 0.001), while transit kinetics k1 and k2 are not significantly affected. On the contrary, in the patients with thyrotoxicosis post-nifedipine Amax was not significantly different from pre-nifedipine study, while k1 was slightly suppressed (p < 0.05) and k2 was significantly elevated (p < 0.01). Apparently different Ca+2 dependent control mechanisms are operative in euthyroid and thyrotoxic states. Clinical implications of these observations have been discussed.