Mechanisms for Plasma Volume Changes in Normal Pregnancy

The precise mechanism(s) for plasma volume expansion during pregnancy remain unexplained. Although 950 mmol of sodium is accumulated and distributed between the products of conception and maternal extracellular volumes in pregnancy, neither changes in the maternal renal handling of sodium nor changes in sodium intake during normal pregnancy correlate with changes in plasma volume. Other suggested mechanisms for the increased plasma volume include increased levels of antinatriuretic factors, such as mineralo-corticoids (aldosterone and deoxycorticosterone), and elevated natriuretic factors, such as oxytocin, prostacyclin, and melanocyte stimulating hormone (MSH). Increased progesterone levels may contribute to antinatriuresis by increasing deoxycorticosterone production via 21-hydroxylation.

Three theories, comprising vascular "underfill," "normal-fill," and "overfill," have also been postulated to explain these observations. The "underfill" theory proposes that the hypervolemia of normal pregnancy is a suboptimal response to the generalized vasodilatation of pregnancy. Evidence in support of this theory includes activation of the renin-angiotensin system and data that adrenectomy and/or sodium restriction are tolerated less well by pregnant rats than by nonpregnant controls. These observations are supported by serial hemodynamic studies of both baboons and women in early pregnancy. The normal-fill theory proposes a continual resetting of volume sensing mechanisms as pregnancy advances, so that the increases in volume are sensed as normal. This theory is supported by evidence that sodium and water excretion by the proximal nephron is unaltered and in pregnancy, urine dilution appears to be normal during fluid overload. Furthermore, the sodium excretory responses to saline infusion are similar in the normal pregnant and nonpregnant states. The "overfill" theory, on the other hand, considers the plasma volume expansion as an epiphenomenon, secondary to factors such as the marked increased in circulating mineralocorticoids. This explanation is supported by the absolute increases in extracellular water volumes, high levels of circulating natriuretic factors, and/or inhibitors of the membrane pump increases in renal hemodynamics and also by increased sodium excretion in response to saline infusions.

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