The role of thyrocalcitonin in calcium homeostasis of rats has been studied in three types of experiments. 1. (a) Measurement of the effect on the blood calcium level, [Ca s], of varying net calcium absorption in normal (N), thyroparathyroidectomized (TPTX) and thyroidectomized animals with autogenous parathyroid transplants (TX). These studies showed that the values of [Ca s] were similar in N and TX animals at all levels of net absorption over a nearly 100-fold range. Moreover, the error, i.e., the difference between [Ca s] when net absorption was zero and when it was very high, was close to zero. In TPTX animals, on the other hand, the values for [Ca s] were markedly lower than in the other two groups at all levels of net absorption and the error of [Ca s] increased linearly and proportionately with increased absorption. 2. (b) Determination of the intensity of the steady-state parameters of calcium metabolism (pool size, rates of Ca absorption, deposition in and removal from bone, urinary output) in N, in controls with parathyroid autografts (C), and in TX failed to reveal any important differences between either N and TX or C and TX. 3. (c) Measurement of the return of [Ca s] to its base value following an acute calcium surcharge by intraperitoneal injection in N, C, and in TX animals indicated a greater delay in the return in the TX than in the C or N animals. It is concluded that thyrocalcitonin is not involved in the regulation of the steady state value of the blood calcium or of the steady-state parameters of calcium metabolism, including turnover and amount of bone calcium. Rather, thyrocalcitonin appears to refine the action of parathyroid hormone in terms of its effects on bone, the primary regulator of blood calcium.