Effect of chronic treatment with estrogen on the dipsogenic response of rats to angiotensin.
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.
D000803:Angiotensin I / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000809:Angiotensins / Q000494:pharmacology*; D000818:Animals; D004326:Drinking / Q000187:drug effects*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D011188:Potassium / Q000652:urine; D051381:Rats; D012964:Sodium / Q000652:urine; D014554:Urination / Q000187:drug effects
D000809:Angiotensins; D000804:Angiotensin II; D004958:Estradiol; D000803:Angiotensin I; D012964:Sodium; D011188:Potassium