Responsiveness to various dipsogenic stimuli in rats treated chronically with norethynodrel, ethinyl estradiol and both combined.
Administration of the estrogen, ethinyl estradiol (36 microng/kg/day), alone, and in combination with the progestogen, norethynodrel (165 microng/kg/day), significantly attenuated the dipsogenic response characteristically induced by acute s.c. administration of the beta adrenergic agonist, dl-iosproterenol (50 microng/kg). Attenuation was apparent within 1 week of steroid treatment, and remained during the 4 weeks of testing. After 16 weeks 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. However, estrogen treatment did not affect drinking after a 24-hour 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. In addition, the reduced dipsogenic response to hypertonic NaCl loading suggests that estrogens may inhibit thirst mechanisms centrally. Dehydration, which combines hypovolemic and osmotic thirst situmul was, however, sufficient to overcome the reduced dipsogenic responsiveness of estrogen-treated rats.[1]References
- Responsiveness to various dipsogenic stimuli in rats treated chronically with norethynodrel, ethinyl estradiol and both combined. Thrasher, T.N., Fregly, M.J. J. Pharmacol. Exp. Ther. (1977) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
