title: Sex differences in osmotic regulation of AVP and renal sodium handling.
abstract: To determine sex differences in osmoregulation of arginine vasopressin (AVP) and body water, we studied eight men (24 +/- 1 yr) and eight women (29 +/- 2 yr) during 3% NaCl infusion [hypertonic saline infusion (HSI); 120 min, 0.1 ml. kg body wt(-1). min(-1)]. Subjects then drank 15 ml/kg body wt over 30 min followed by 60 min of rest. Women were studied in the early follicular (F; 16.1 +/- 2.8 pg/ml plasma 17beta-estradiol and 0.6 +/- 0.1 ng/ml plasma progesterone) and midluteal (L; 80.6 +/- 11.4 pg/ml plasma 17beta-estradiol and 12.7 +/- 0.7 ng/ml plasma progesterone) menstrual phases. Basal plasma osmolality was higher in F (286 +/- 1 mosmol/kgH(2)O) and in men (289 +/- 1 mosmol/kgH(2)O) compared with L (280 +/- 1 mosmol/kgH(2)O, P < 0.05). Neither menstrual phase nor gender affected basal plasma AVP concentration (P([AVP]); 1.7 +/- 4, 1.9 +/- 0.4, and 2.2 +/- 0.5 pg/ml for F, L, and men, respectively). The plasma osmolality threshold for AVP release was lowest in L (x-intercept, 263 +/- 3 mosmol/kgH(2)O, P < 0.05) compared with F (273 +/- 2 mosmol/kgH(2)O) and men (270 +/- 4 mosmol/kgH(2)O) during HSI. Men had greater P([AVP])-plasma osmolality slopes (i.e., sensitivity) compared with F and L (slopes = 0.14 +/- 0.04, 0.09 +/- 0.01, and 0.24 +/- 0.07 for F, L, and men, respectively, P < 0.05). Despite similar Na+-regulating hormone responses, men excreted less Na+ during HSI (0.7 +/- 0.1, 0.7 +/- 0.1, and 0.5 +/- 0.1 meq/kg body wt for F, L, and men, respectively, P < 0.05). Furthermore, men had greater systolic blood pressure (119 +/- 5, 119 +/- 5, and 132 +/- 3 mmHg for F, L, and men, respectively, P < 0.05) than F and L. Our data indicate greater sensitivity in P([AVP]) response to changes in plasma osmolality as the primary difference between men and women during HSI. In men, this greater sensitivity was associated with an increase in systolic blood pressure and pulse pressure during HSI, most likely due to a shift in the pressure-natriuresis curve.
authors.affiliation: The John B. Pierce Laboratory, Yale University School of Medicine, 290 Congress Ave., New Haven, Connecticut 06519, USA. nstach@jbpierce.org
authors.forename: N S
authors.initials: NS
authors.lastname: Stachenfeld
authors.forename: A E
authors.initials: AE
authors.lastname: Splenser
authors.forename: W L
authors.initials: WL
authors.lastname: Calzone
authors.forename: M P
authors.initials: MP
authors.lastname: Taylor
authors.forename: D L
authors.initials: DL
authors.lastname: Keefe
mesh_terms: D000328:Adult; D000465:Algorithms; D001127:Arginine Vasopressin / Q000235:genetics / Q000502:physiology*; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology; D001834:Body Water / Q000187:drug effects / Q000502:physiology; D005260:Female; D016678:Genome; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D008297:Male; D012083:Renin / Q000097:blood; D012727:Sex Characteristics; D012964:Sodium / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000235:genetics / Q000502:physiology*
chemical_list: D006454:Hemoglobins; D001127:Arginine Vasopressin; D012964:Sodium; D012083:Renin