Estrogen influences osmotic secretion of AVP and body water balance in postmenopausal women.

To determine if estrogen upregulates osmotic secretion of arginine vasopressin (AVP) and alters body water balance, we infused hypertonic (3% NaCl) saline in 6 women (68 ± 3 yr) after 14 days of 17β-estradiol (transdermal patch, ∼0.1 mg/day, E2) and placebo (control) administration. Hypertonic saline was infused at 0.1 ml ⋅ kg-1 ⋅ min-1for 120 min, and after a 30-min equilibration period, the subjects drank water ad libitum for 180 min. E2 increased basal plasma estradiol concentration from ≤12 to 80 ± 12 pg/ml and plasma AVP concentration (P[AVP]) from 2.1 ± 0.7 to 3.1 ± 0.8 pg/ml ( P< 0.05), but not plasma osmolality (Posm, 288 ± 1 and 287 ± 1, for control and E2, respectively). Hypertonic saline infusion increased Posm by 18 ± 1 and 17 ± 1 mosmol/kgH2O and P[AVP] by 5.2 ± 0.5 and 4.9 ± 0.4 pg/ml for control and E2 treatments, respectively. The P[AVP]-Posmrelationship shifted upward after E2, with no change in sensitivity (slope, 0.36 ± 0.02 and 0.33 ± 0.03 pg ⋅ ml-1 ⋅ mosmol-1for control and E2, respectively). Water intake was similar between control and E2 (24 vs. 22 ml/kg), but by 180 min of drinking, urine output and free water clearance ([Formula: see text]) were reduced by 5.6 ± 2.3 ml/kg and 2.6 ± 2.0 ml/min, respectively ( P < 0.05) after E2. Plasma aldosterone concentration was unaffected by E2, but fractional sodium excretion was reduced from 2.7 ± 0.5 to 1.7 ± 0.4% ( P < 0.05) at 180 min of drinking. Our data suggest that E2augments osmotic AVP secretion, thereby implicating elevated AVP as a contributor to water retention in high E2 states; however, an increase in renal sodium reabsorption was a major component of the enhanced fluid retention.