Stachenfeld NS. Sex hormone effects on body fluid regulation. Exerc Sport Sci Rev 2008;36(3):152-9. Sex Hormone Effects on Body Fluid Regulation
In young women, estradiol and progesterone primarily control reproduction, but they also affect fluid regulation.
Estradiol lowers the operating point for osmoregulation of arginine vasopressin and thirst and increases plasma volume.
Although total body water and sodium content are only mildly affected, data presented in this article suggest that reproductive hormones alter homeostatic set points for body fluid and tonicity.
Stachenfeld NS, Keefe DL. Estrogen effects on osmotic regulation of AVP and fluid balance. Am J Physiol Endocrinol Metab 2002;283(4):E711-21. http://ajpendo.physiology.org/content/283/4/E711 (Estrogen effects on osmotic regulation of AVP and fluid balance | Endocrinology and Metabolism)
To determine estrogen effects on osmotic regulation of arginine vasopressin (AVP) and body fluids, we suppressed endogenous estrogen and progesterone using the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate (GnRHa).
Subjects were assigned to one of two groups:
1) GnRHa alone, then GnRHa + estrogen (E, n = 9, 25 +/- 1 yr);
2) GnRHa alone, then GnRHa + estrogen with progesterone (E/P, n = 6, 26 +/- 3).
During GnRHa alone and with hormone treatment, we compared AVP and body fluid regulatory responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml. min(-1). kg body wt(-1)), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest).
Plasma [E(2)] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P(4)] increased from 0.6 to 5.7 ng/ml during E/P and was unchanged (0.4 to 0.6 ng/ml) during E.
Compared with GnRHa alone, E reduced osmotic AVP release threshold (275 +/- 4 to 271 +/- 4 mosmol/kg, P < 0.05), and E/P reduced the AVP increase in response during HSI (6.0 +/- 1.3 to 4.2 +/- 0.6 pg/ml at the end of HSI), but free water clearance was unaffected in either group.
Relative to GnRHa, pre-HSI plasma renin activity (PRA) was greater during E (0.8 +/- 0.1 vs. 1.2 +/- 0.2 ng ANG I. ml(-1). h(-1)) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 +/- 0.2 vs. 2.5 +/- 0.6) and after HSI (0.6 +/- 0.1 vs. 1.1 +/- 1.1) and recovery (0.5 +/- 0.1 vs. 1.3 +/- 0.2 ng ANG I. ml(-1). h(-1)).
Baseline fractional excretion of sodium was unaffected by E or E/P but was attenuated by the end of recovery for both E (3.3 +/- 0.6 vs. 2.4 +/- 0.4%) and E/P (2.8 +/- 0.4 vs 1.7 +/- 0.4%, GnRHa alone and with hormone treatment, respectively).
Fluid retention increased with both hormone treatments.
Renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium excretion. E/P increased sodium retention and renin-angiotensin-aldosterone stimulation.
