Experiments were performed with adult male rats to assess the hypothalamic-pituitary-gonadal system in 131I- and propylthiouracil-induced hypothyroidism. Hypothyroidism resulted in no difference in testis weights although both the seminal vesicles and ventral prostates were significantly smaller in hypothyroid rats. In the basal state TSH [thyroid stimulating hormone] was highly elevated in hypothyroid animals, T4 [thyroxine] was lowered, and LH [luteinizing hormone], FSH [follicle stimulating hormone], and testosterone were unchanged. LHRH [luteinizing hormone releasing hormone] (100 ng/100 g BW [body wt.] i.p.) and castration caused a significantly greater rise of both serum LH and FHS in hypothyroid than in euthyroid rats. A similar rise in serum and testis testosterone occurred in hypothyroid and euthyroid animals after a single bolus of LH (30 .mu.g/100 g GW). Androgen responsiveness of the sex accessory glands and the feedback sensitivity on LH and FSH release from the pituitary were assessed after administration of graded doses of testosterone to castrate hypothyroid and euthyroid rats. The weight response curves for both the seminal vesicles and ventral prostates were parallel in hypothyroid and euthyroid animals, indicating no difference in testosterone responsiveness of the organs. The same dose of testosterone (250 .mu.g/100 g BW daily) was needed in both hypothyroid and euthyroid rats to suppress the high castration levels of serum LH and FSH, which suggested no major change in the feedback sensitivity of the hypothalamic-pituitary axis to testosterone. These studies demonstrate that hypothyroidism results in higher serum radioimmunoassayable gonadotropin levels in response to castration and LHRH administration. The peripheral segments of the reproductive system, the testes and sex accessories, do not have altered responses to LH and testosterone, respectively.