8 Volume homeostasis and osmoregulation in human pregnancy

https://doi.org/10.1016/S0950-351X(89)80011-4Get rights and content

Summary

This chapter reviews alterations in volume and sodium homeostasis and osmoregulation during human pregnancy. Pregnant women undergo extracellular and plasma volume increases of 50–70%, and these changes accompany marked cumulative sodium retention shared by both mother and fetus. Pregnancy alters several factors with opposing effects on renal salt handling; however, mechanisms by which gestational sodium accumulation and volume expansion are achieved remain obscure. Furthermore, despite substantial increases in absolute blood volume, considerable uncertainty exists as to how this volume is sensed, particularly in late pregnancy when a rapid increase in volume is associated with decreases in peripheral resistance and blood pressure. Attempts to assess ‘effective’ intravascular volume suggest that pregnant women sense their volume as normal.

Osmoregulation is also changed. Body tonicity and the osmotic thresholds for AVP release and thirst decrease by about 10 mosm/kg. The mechanisms responsible for the osmoregulatory changes are obscure. Haemodynamic stimuli such as decrements in blood pressure and of ‘effective circulating volume’ do not seem to account for them. Of the many increments in hormone levels known to accompany gestation, only hCG has so far been implicated in these changes.

Pregnant women experience three- to fourfold increments in AVP disposal rates between early and mid pregnancy; this may be caused by the striking rise in circulating cystine-aminopeptidase (vasopressinase) which also occurs during this period. The increments in MCR may be one reason why the hormonal response to a given osmotic stimulus appears to decrease in late pregnancy.

All these alterations permit speculation on the manner in which the decrease in Posm occurs and is maintained within narrow limits. Lowering the osmotic threshold to drink stimulates a rise in water intake and dilution of body fluids. Since AVP release is not suppressed at the usual level of hypotonicity, AVP continues to circulate at levels sufficient to permit water retention. Posm continues to decline until it decreases below the new osmotic thirst threshold, when a new steady state is established. At this point water turnover, too, resembles that in the non-pregnant state.

The change in MCR and the marked increment in plasma vasopressinase may explain certain observations regarding disordered water metabolism during late pregnancy. These are the transient DI syndromes due either to subclinical hypothalamic disease or to a disorder peculiar to pregnancy which is AVP-resistant but dDAVP-responsive; the latter analogue resists degradation by vasopressinase.

References (92)

  • AitkenJM et al.

    The redistribution of body sodium in women on long-term oestrogen therapy

    Clinical Science and Molecular Medicine

    (1984)
  • AspillagaMO et al.

    Some new aspects of the endocrinological response to pregnancy

    British Journal of Obstetrics and Gynaecology

    (1983)
  • BarronWM et al.

    Osmoregulation in pseudopregnant and prolactin-treated rats: comparison with normal gestation

    American Journal of Physiology

    (1988)
  • BarronWM et al.

    Role of volume in the regulation of vasopressin secretion during pregnancy in the rat

    Journal of Clinical Investigation

    (1984)
  • BarronWM et al.

    Transient vasopressin-resistant diabetes insipidus of pregnancy

    New England Journal of Medicine

    (1984)
  • BarronWM et al.

    Effect of ovarian sex steroids on osmoregulation and vasopressin secretion in the rat

    American Journal of Physiology

    (1986)
  • BarronWM et al.

    Role of hemodynamic factors in the osmoregulatory alterations of rat pregnancy

    American Journal of Physiology

    (1989)
  • BayWH et al.

    Factors controlling plasma renin and aldosterone during pregnancy

    Hypertension

    (1979)
  • BaylisC

    Glomerular filtration and volume regulation in gravid animal models

    Clinical Obstetrics and Gynaecology

    (1987)
  • BaylisPH

    Vasopressin secretion during the menstrual cycle: an overview

  • BaylisPH

    Osmoregulation and control of vasopressin secretion in healthy humans

    American Journal of Physiology

    (1988)
  • BaylisPH et al.

    Recurrent pregnancy-induced polyuria and thirst due to hypothalamic diabetes insipidus: an investigation into possible mechanisms responsible for polyuria

    Clinical Endocrinology

    (1986)
  • BeardwellCG et al.

    Radioimmunoassay of plasma vasopressin in physiological and pathological states in man

    Journal of Endocrinology

    (1973)
  • Broughton-PipkinF

    The renin—angiotensin system in normal and hypertensive pregnancies

  • BrownMA

    Sodium and plasma volume regulation in normal and hypertensive pregnancy: a review of physiological and clinical implications

    Clinical and Experimental Hypertension

    (1989)
  • BrownMA et al.

    The effects of intravenous angiotensin II upon blood pressure and sodium and urate excretion in human pregnancy

    Journal of Hypertension

    (1988)
  • CaseyML et al.

    Metabolism of deoxycorticosterone and deoxycortisterone sulfate in men and women

    Journal of Clinical Investigation

    (1982)
  • ChesleyLC et al.

    Renal hemodynamics and intravascular volume in normal and hypertensive pregnancy

  • ChurchillSE et al.

    Sodium balance during pregnancy in the rat

    American Journal of Physiology

    (1980)
  • CollinsR et al.

    Overview of randomised trials of diuretics in pregnancy

    British Medical Journal

    (1985)
  • DavisonJM et al.

    Plasma osmolality and urinary concentration and dilution during and after pregnancy: evidence that lateral recumbency inhibits maximal urinary concentrating ability

    British Journal of Obstetrics and Gynaecology

    (1981)
  • DavisonJM et al.

    Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy

    American Journal of Physiology

    (1984)
  • DavisonJM et al.

    Serial evaluation of vasopressin release and thirst in human pregnancy. Role of human chorionic gonadotropin on the osmoregulatory changes of gestation

    Journal of Clinical Investigation

    (1988)
  • DavisonJM et al.

    Suppression of AVP release by drinking despite hypertonicity during and after gestation

    American Journal of Physiology

    (1988)
  • DavisonJM et al.

    Changes in the metabolic clearance of vasopressin and of plasma vasopressinase throughout human pregnancy

    Journal of Clinical Investigation

    (1989)
  • DavisonJM et al.

    Metabolic clearance rates of arginine vasopressin and 1-deamino,8-D-AVP (dDAVP) in human pregnancy: evidence that placental enzymes increase MCR of AVP in gestation

    Clinical Research

    (1989)
  • DavisonJM et al.

    Humoral and volume effects on osmoregulation in pregnancy

    Kidney International

    (1989)
  • DevaneGW

    Vasopressin levels during pregnancy and labor

    Journal of Reproductive Medicine

    (1985)
  • DurrJA

    Diabetes insipidus syndromes of pregnancy

  • DurrJA et al.

    Diabetes insipidus in pregnancy associated with abnormally high circulating vasopressinase activity

    New England Journal of Medicine

    (1987)
  • EdwardsCRW et al.

    Vasopressin analogue DDAVP in diabetes insipidus. Clinical and laboratory studies

    British Medical Journal

    (1973)
  • EganB et al.

    Role of cardiopulmonary receptors in ADH release in normal humans

    Hypertension

    (1984)
  • FordSM

    Transient vasopressin-resistant diabetes insipidus of pregnancy

    Obstetrics and Gynecology

    (1986)
  • FordSM et al.

    Transient vasopressin-resistant diabetes insipidus of pregnancy

    Obstetrics and Gynecology

    (1986)
  • FriedmanSA

    Preeclampsia: a review of the role of prostaglandins

    Obstetrics and Gynecology

    (1988)
  • GalleryEDM

    Volume homeostasis in normal and hypertensive human pregnancy

  • Cited by (35)

    • Ocular changes during pregnancy

      2018, Journal of Current Ophthalmology
      Citation Excerpt :

      The mechanism presumably is related to hormonal changes such as low progesterone levels; however, by the third trimester, an increase in progesterone and aqueous outflow often result in decreased or absence of Krukenberg spindles.17 Water retention is a well-described phenomenon in pregnancy.18 At the ocular level, the increased aqueous component can result in corneal edema and contact lens intolerance.3

    • Reproductive and developmental toxicity of potassium perfluorohexanesulfonate in CD-1 mice

      2018, Reproductive Toxicology
      Citation Excerpt :

      Interestingly, PFHxS was less potent than PFOS and this may explain, in part, the absence of postnatal mortality in pups born to dams that were exposed to K+PFHxS. Although the toxicokinetics of PFHxS during pregnancy have not been fully characterized in mice, it is expected that, under daily treatment of K+PFHxS during gestation, the resulting maternal serum PFHxS concentrations would be subject to some degree of dilution due to pregnancy-induced plasma expansion [75,76], as demonstrated by the reduction in F0 female serum PFHxS concentrations on GD18 when compared to pre-gestation serum PFHxS concentrations on SD 14. In addition, the difference in serum PFHxS concentrations before and after gestation in F0 dams also offered compelling evidence for the occurrence of in utero transfer in that pooled fetal serum PFHxS concentrations obtained on GD 18 were comparable to the respective maternal serum PFHxS concentrations.

    • Normative bladder diary measurements in pregnant women

      2017, European Journal of Obstetrics and Gynecology and Reproductive Biology
      Citation Excerpt :

      Analysis of the within-trimester diary completion times revealed that 83% of our first trimester diaries were completed late in the trimester (11–12 weeks). Human and animal studies [12] suggest that in pregnancy TBW accretion increases until about 8 weeks after gestation, at which time accretion stops with TBW having increased 7–8 L (L). Thus, published data are compatible with a hypothetical V24 increase early in pregnancy.

    • Heart Disease in Pregnancy

      2016, Obstetrics: Normal and Problem Pregnancies
    • Cardiovascular Medications in Pregnancy

      2013, Clinical Pharmacology During Pregnancy
    • Cardiovascular Medications in Pregnancy

      2012, Clinical Pharmacology During Pregnancy
    View all citing articles on Scopus

    This work was supported by the Medical Research Council (UK) and the National Institutes of Health (USA).

    View full text