Pregnancy: an overfill or underfill state

Abstract

With pregnancy, the expansion of plasma and extracellular fluid volume, increased cardiac output, and increased glomerular filtration rate (GFR) and renal blood flow (RBF) are compatible with primary renal sodium and water retention with secondary enlargement of the vascular compartment (overfill hypothesis). Alternatively, a primary enlargement of the vascular compartment (eg, prostaglandin-mediated vasodilation and placental arteriovenous shunting) with secondary renal sodium and water retention (underfill hypothesis) is supported by the activation of the renin-angiotensin-aldosterone (RAA) system, resetting of vasopressin release and thirst to a lower plasma osmolality, and a further stimulation of the RAA system and vasopressin when pregnant rats' water intake is maintained at a level of a virgin rat fluid intake, diminished BP and increased cardiac output in the first trimester, and worsening of hyponatremia with sodium restriction in the pregnant but not the virgin rat. With the underfill hypothesis, normal sodium and water excretion with mineralocorticoid escape could be mediated by hormonally induced increases in GFR and RBF associated with pregnancy. The nature of such a hormone effect of pregnancy to enhance renal hemodynamics remains to be defined.