Variation in Osmoregulation of Arginine Vasopressin During the Human Menstrual Cycle

Abstract

Osmoregulation of vasopressin secretion was studied in eight healthy women in the follicular and luteal phases of the menstrual cycle. Basal plasma osmolality in the luteal phase was significantly lower than in the follicular period (282.4 +/- 0.6, 285.6 +/- 1.1mmol/kg, respectively, P less than 0.05). Plasma AVP (pAVP) and plasma osmolality (pOsm) were measured during the infusion of 850 mmol/l saline in both phases of the cycle, and linear regression analyses of these data gave the following regression equations (i) follicular, pAVP = 0.43 (pOsm - 284), r = + 0.93, (ii) luteal, pAVP = 0.31 (pOsm - 279), r = + 0.95. Both the slope and abscissal intercept were significantly different (P less than 0.01). Osmotic threshold for thirst sensation in the luteal phase was lower than the follicular (293 +/- 2,297 +/- 1 mmol/kg, P less than 0.005). We conclude that, in the luteal phase, the threshold for AVP release and the gain or sensitivity of the osmostat are reduced together with lowering of the thirst threshold, which account for the lower basal luteal plasma osmolality.

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

“…Careful investigation by Spruce et al ( 1985) identified subtle variations during the normal menstrual cycle, but failed to confirm fluctuations in plasma vasopressin concentration in the cycle (Forsling et al, 1981). Small decrements in plasma osmolality of the order of 2-3 mOsm/kg were noted in the luteal phase of ovulatory cycles, which was due principally to a reduction in the osmotic thresholds for vasopressin secretion and thirst.…”

Endogenous and exogenous female sex hormones and renal electrolyte handling: effects of an acute sodium load on plasma volume at rest

“…In humans, it has been established that basal Posm is higher in the follicular than in the luteal phase, with the threshold for AVP release lowest in the luteal phase (29,(31)(32). Moreover, estrogens upregulate the number of AVP binding sites (28,32,38), which increase the pressor response in the renal vascular bed. These observations are further supported by the result of the present study.…”

“…Primarily, it is known that estrogens favor fluid retention by activating the renin-angiotensin-aldosterone system and that progesterone is able to antagonize this event (21). Estrogen enhances vasodilation and capillary permeability and acts centrally to lower the operating set point of plasma osmolality (Posm) (a leftward shift in AVP sensitivity) (21,22,28,30,38). Progesterone competes directly with the same mineralocorticoid receptor as aldosterone, which may cause a transient natriuresis (20).…”

Estrogen receptors: Their roles in regulation of vasopressin release for maintenance of fluid and electrolyte homeostasis

“…Although the impact on VP secretion of activation of these specific ERs has not been evaluated, a consistent finding reported in the literature is that the osmotic threshold for VP release and thirst fluctuates with physiological changes in circulating estrogen. The osmotic threshold for VP release is lower in the midluteal phase compared to the midfollicular phase of the menstrual cycle [80,81,94], and in both humans and rats the osmotic threshold for VP secretion is lower during gestation [15]. In rats, ovariectomy reduced the VP response to a hypertonic stimulus and the response was restored by estrogen treatment [24].…”

“…In addition, fluid retention is frequently an unpleasant side effect of the use of gonadal steroids for contraception or hormone replacement therapy. It is well established that the osmotic threshold for vasopressin (VP) secretion is reset during pregnancy and during the luteal phase of the menstrual cycle [13,15,80,81,94]. Furthermore, women astronauts are more susceptible to orthostatic hypotension following extended weightlessness [99].…”