Female rats treated with estradiol benzoate for 23 weeks at doses of 25 and 44 microgram/kg/day had an attenuated drinking response to peripheral administration of graded doses of angiotensin I and angiotensin II. No significant difference between the responses of the two estrogen-treated groups was observed, suggesting that maximal attenuation had been attained with the lower dose. Angiotensin II (50, 100 and 200 microgram/kg, IP) increased urine output and urinary sodium excretion rate in a graded fashion with increasing doses in both control and estrogen-treated rats. However, the latter had a somewhat greater response. Administration of angiotensin I (50, 100 and 200 microgram/kg, SC) had a similar, but less consistent, effect on urine output and urinary sodium excretion rate in both control and estrogen-treated groups. The attenuated drinking response of estrogen-treated rats to angiotensin I and angiotensin II suggests either that administered angiotensin failed to gain access to the brain or that central receptors mediating thirst are less sensitive in estrogen-treated rats. The present studies fail to distinguish between these possibilities.