• 1 January 1977
    • journal article
    • research article
    • Vol. 201  (1) , 84-91
Abstract
Administration of the estrogen, ethinyl estradiol (36 .mu.g/kg per day), alone, and in combinattion with the progestogen, norethynodrel (165 .mu.g/kg per day), significantly attenuated the dipsogenic response characteristically induced by acute s.c. administration of the .beta.-adrenergic agonist, dl-isoproterenol (50 .mu.g/kg). Attenuation was apparent within 1 wk of steroid treatment and remained during the 4 wk of testing. After 16 wk of steroid treatment, the drinking response to acute i.p. administration of renin (2 and 4 Goldblatt units/rat) was tested. The groups receiving ethinyl estradiol alone, and in combination with norethynodrel, but not norethynodrel alone, showed a reduced water intake compared with untreated controls. Drinking induced by administration of hypertonic saline (1% of body weight of 1 M NaCl solution, i.p.) was also reduced in rats treated with the estrogenic, but not the progestational, agent. Estrogen treatment did not affect drinking after a 24 h period of dehydration. Although the reduced dipsogenic response to isoproterenol observed in estrogen-treated rats may reflect a reduced renin secretion, drinking could not be induced in these animals by administration of renin. The reduced dipsogenic response to hypertonic NaCl loading suggests that estrogens may inhibit thirst mechanisms centrally. Dehydration, which combines hypovolemic and osmotic thirst stimuli was, however, sufficient to overcome the reduced dipsogenic responsiveness of estrogen-treated rats.