Estrogen effects on osmotic regulation of AVP and fluid balance

Abstract

Stachenfeld, Nina S., and David L. Keefe. Estrogen effects on osmotic regulation of AVP and fluid balance. Am J Physiol Endocrinol Metab 283: E711-E721, 2002; 10.1152/ ajpendo.00192.2002To 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 ϩ estrogen (E, n ϭ 9, 25 Ϯ 1 yr); 2) GnRHa alone, then GnRHa ϩ estrogen with progesterone (E/P, n ϭ 6, 26 Ϯ 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 ⅐ min Ϫ1 ⅐ kg body wt Ϫ1 ), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest). Plasma [E2] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P4] 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 Ϯ 4 to 271 Ϯ 4 mosmol/kg, P Ͻ 0.05), and E/P reduced the AVP increase in response during HSI (6.0 Ϯ 1.3 to 4.2 Ϯ 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 Ϯ 0.1 vs. 1.2 Ϯ 0.2 ng ANG I ⅐ ml Ϫ1 ⅐ h Ϫ1 ) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 Ϯ 0.2 vs. 2.5 Ϯ 0.6) and after HSI (0.6 Ϯ 0.1 vs. 1.1 Ϯ 1.1) and recovery (0.5 Ϯ 0.1 vs. 1.3 Ϯ 0.2 ng ANG I ⅐ ml Ϫ1 ⅐ h Ϫ1 ). 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 Ϯ 0.6 vs. 2.4 Ϯ 0.4%) and E/P (2.8 Ϯ 0.4 vs 1.7 Ϯ 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. body fluid regulation; arginine vasopressin; osmolality; thirst; gonadotropin-releasing hormone agonist; luprolide acetate CARDIOVASCULAR DISEASE-RELATED morbidity and mortality are lower in women than in men throughout middle age (8,22), and this risk "advantage" is often attributed to estrogen. Arginine vasopressin (AVP) may be another key hormone involved in these gender differences. AVP is an important hormone involved in fluid balance and blood pressure regulation. AVP is synthesized in the cell bodies of the paraventricular (PVN) and supraoptic (SON) nuclei, located in the anterior hypothalamus. Axons from these areas project into the posterior pituitary, where AVP is stored and released in response to stimulation of central osmoreceptors.Estrogen receptors are present in the PVN and SON of both animals (17, 33) and humans (19), and a number of studies have demonstrated sex differences in AVP neuron size in these nuclei (20,21).Resting pla...

Female sex hormones are associated with the reduction of serum sodium and hypertension complications in patients with aldosterone-producing adenoma

“…Previous studies have observed increased sodium loss in the presence of elevated estrogen and progesterone [45]. Estrogen and progesterone levels may result in increased release of arginine vasopressin [46]. Furthermore, reduced Na + -K + ATPase pump activity by estrogens was observed in female rats [47].…”

Neonatal growth and breast cancer risk in adulthood

“…Our explanation of the association of immediate postnatal weight reduction with breast cancer risk invokes higher levels of pregnancy hormones, including oestrogens, on the basis of well-known properties of these hormones (Stachenfeld and Keefe, 2002;Gomella et al, 2004;Stachenfeld and Taylor, 2004).…”

“…The decline is likely to reflect the extent of water retention by the newborn at the time of delivery, under the influence of pregnancy hormones, including oestrogens (Stachenfeld and Keefe, 2002;Gomella et al, 2004;Stachenfeld and Taylor, 2004). The rate of weight gain after the nadir is influenced by growth factors, notably the IGF system and its determinants (Albertsson-Wikland et al, 1998;Ogilvy-Stuart et al, 1998;Hikino et al, 2001;Skalkidou et al 2003).…”

Patterns of Ecstasy-Associated Hyponatremia in California

“…Tamoxifen, a selective estrogen receptor modulator (SERM) with competitive partial agonist inhibitor effects at the estrogen receptor, decreased plasma ADH levels in rats (33). Estrogen has also been shown to enhance ADH secretion by decreasing the osmotic ADH release threshold, or set point, in humans (34). In rats, estrogen has been shown to reduce the antidiuretic response to ADH (35), however, this effect has not been established in humans.…”