{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:49:45Z","timestamp":1791229785523,"version":"4.1.0"},"reference-count":26,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1999,9,1]]},"abstract":"<jats:p>\n                    To test the hypothesis that estrogen reduces the operating point for osmoregulation of arginine vasopressin (AVP), thirst, and body water balance, we studied nine women (25 \u00b1 1 yr) during 150 min of dehydrating exercise followed by 180 min of ad libitum rehydration. Subjects were tested six different times, during the early-follicular (twice) and midluteal (twice) menstrual phases and after 4 wk of combined [estradiol-norethindrone (progestin), OC E + P] and 4 wk of norethindrone (progestin only, OC P) oral contraceptive administration, in a randomized crossover design. Basal plasma osmolality (P\n                    <jats:sub>osm<\/jats:sub>\n                    ) was lower in the luteal phase (281 \u00b1 1 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O, combined means, P &lt; 0.05), OC E + P (281 \u00b1 1 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O, P &lt; 0.05), and OC P (282 \u00b1 1 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O, P &lt; 0.05) than in the follicular phase (286 \u00b1 1 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O, combined means). High plasma estradiol concentration lowered the P\n                    <jats:sub>osm<\/jats:sub>\n                    threshold for AVP release during the luteal phase and during OC E + P [ x-intercepts, 282 \u00b1 2, 278 \u00b1 2, 276 \u00b1 2, and 280 \u00b1 2 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O, for follicular, luteal (combined means), OC E + P, and OC P, respectively; P &lt; 0.05, luteal phase and OC E + P vs. follicular phase] during exercise dehydration, and 17\u03b2-estradiol administration lowered the P\n                    <jats:sub>osm<\/jats:sub>\n                    threshold for thirst stimulation [ x-intercepts, 280 \u00b1 2, 279 \u00b1 2, 276 \u00b1 2, and 280 \u00b1 2 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O for follicular, luteal, OC E + P, and OC P, respectively; P &lt; 0.05, OC E + P vs. follicular phase], without affecting body fluid balance. When plasma 17\u03b2-estradiol concentration was high, P\n                    <jats:sub>osm<\/jats:sub>\n                    was low throughout rest, exercise, and rehydration, but plasma arginine vasopressin concentration, thirst, and body fluid retention were unchanged, indicating a lowering of the osmotic operating point for body fluid regulation.\n                  <\/jats:p>","DOI":"10.1152\/jappl.1999.87.3.1016","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:18:18Z","timestamp":1513937898000},"page":"1016-1025","source":"Crossref","is-referenced-by-count":121,"title":["Effects of oral contraceptives  on body fluid regulation"],"prefix":"10.1152","volume":"87","author":[{"given":"Nina S.","family":"Stachenfeld","sequence":"first","affiliation":[{"name":"The John B. Pierce Laboratory, Department of Epidemiology and Public Health, and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and Women and Infants Hospital, Brown University School of Medicine, Providence, Rhode Island 02905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Celso","family":"Silva","sequence":"additional","affiliation":[{"name":"The John B. Pierce Laboratory, Department of Epidemiology and Public Health, and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and Women and Infants Hospital, Brown University School of Medicine, Providence, Rhode Island 02905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L.","family":"Keefe","sequence":"additional","affiliation":[{"name":"The John B. Pierce Laboratory, Department of Epidemiology and Public Health, and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and Women and Infants Hospital, Brown University School of Medicine, Providence, Rhode Island 02905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheryl A.","family":"Kokoszka","sequence":"additional","affiliation":[{"name":"The John B. Pierce Laboratory, Department of Epidemiology and Public Health, and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and Women and Infants Hospital, Brown University School of Medicine, Providence, Rhode Island 02905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ethan R.","family":"Nadel","sequence":"additional","affiliation":[{"name":"The John B. Pierce Laboratory, Department of Epidemiology and Public Health, and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519; and Women and Infants Hospital, Brown University School of Medicine, Providence, Rhode Island 02905"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"issue":"27","key":"B1","first-page":"R924","volume":"258","author":"Akaishi T.","year":"1990","journal-title":"Am. J. Physiol."},{"issue":"13","key":"B2","first-page":"E352","volume":"250","author":"Barron W. M.","year":"1986","journal-title":"Am. J. Physiol."},{"issue":"24","key":"B3","first-page":"E252","volume":"261","author":"Clark B. A.","year":"1991","journal-title":"Am. J. 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