Peripheral arterial vasodilation hypothesis of sodium and water retention in pregnancy: implications for pathogenesis of preeclampsia-eclampsia. Primary peripheral arterial vasodilation with relative underfilling of the arterial circulation occurs in early pregnancy and leads to several consequences, including decreased systolic and diastolic blood pressures, enhanced cardiac output secondary to afterload reduction, stimulation of the renin-angiotensin-aldosterone axis, nonosmotic stimulation of thirst and vasopressin release, and renal sodium and water retention with expansion of the extracellular fluid and plasma volume compartments. These are events known to occur in all states of arterial vasodilation. Pregnancy has, however, several unique features. Primary arterial vasodilation generally is associated with no change or a decrease in renal blood flow and glomerular filtration rate and failure to escape from the sodium-retaining effects of aldosterone. In early pregnancy, renal blood flow and glomerular filtration rate increase by 30-50% in parallel with the peripheral arterial vasodilation but before plasma volume expansion. No known vasodilator exhibits such a profound effect on renal hemodynamics. Vasodilating prostaglandins may contribute to, but cannot explain, this remarkable enhancement of renal hemodynamics in early pregnancy. Therefore, a highly potent, as yet undefined, systemic and renal vasodilator must be unique to pregnancy. The increased glomerular filtration rate and filtered sodium load with enhanced distal tubular sodium delivery allows escape from aldosterone, an effect not observed in other states of arterial underfilling. This vasodilator may also account, at least in part, for the vascular resistance to angiotensin known to occur in normal pregnancy. This hypothesis for the normal physiology of pregnancy sets the stage for understanding the pathogenesis of preeclampsia-eclampsia. 